ADFM National Alzheimer's Caregivers Network Malaysia

AN ALZHEIMER'S VALENTINE

2012-02-14T16:10:00.001+08:00

(Source: By Tom and Karen Brenner, Alzheimer's Reading Room)

We were impossibly young and so beautiful,
When we met and fell in love.

You were the cool guy from the big city
I was the shy small town girl.

I bring you photographs of those days long ago,
You look and smile and ask me who those people are.

I take your hand. It is warm and strong in mine,
You don’t remember me but you know that we belong together.

I tell you the stories of those two young people
You listen intently and study their faces.

And look into my face,
With wonder in your eyes.

I have come to understand that it doesn't matter,
That you no longer remember who we were then.

It only matters that we can sit and hold hands,
While I tell you stories of our past.

Like an old photograph, memory can fade away,
But love endures.

In the touch of hands, in a smile,
In the wonder I see in your eyes.

Memory Gate Opened by Deep Brain Stimulation

2012-02-14T00:30:00.005+08:00

Could a small jolt to the brain be the answer to memory loss?
A new study at UCLA may raise hopes for those suffering from the effects of Alzheimer's and other brain-diminishing diseases. In a small sampling, seven patients with epilepsy—including some with memory impairment—had wires inserted into their brains, delivering electrical current to clusters of neurons that no longer function properly and cause seizures. In the process, researchers noted that all seven patients also exhibited improved memory, allowing them to navigate a virtual taxi cab through a computer-generated town created for the study.
Although very preliminary, the experiment saw improvement even in those patients not suffering from memory impairment, indicating that this stimulating technique might also benefit those with perfect cognitive functioning.
Now, if it could only help us find our car keys.
_________________________________________________________________________________

Have you ever gone to the movies and forgotten where you parked the car? New UCLA research may one day help you improve your memory.

UCLA neuroscientists have demonstrated that they can strengthen memory in human patients, by stimulating a critical junction in the brain. Published in the Feb. 9 2012 Edition of the New England Journal of Medicine, the finding could lead to a new method for boosting memory in patients with early Alzheimer's disease.

The UCLA team focused on a brain site called the entorhinal cortex. Considered the doorway to the hippocampus, which helps form and store memories, the entorhinal cortex plays a crucial role in transforming daily experience into lasting memories.

"The entorhinal cortex is the golden gate to the brain's memory mainframe," said senior author Dr. Itzhak Fried, a professor of neurosurgery at the David Geffen School of Medicine at UCLA. "Every visual and sensory experience that we eventually commit to memory funnels through that doorway to the hippocampus. Our brain cells must send signals through this hub in order to form memories that we can later consciously recall."

Fried and his colleagues followed seven epilepsy patients who already had electrodes implanted in their brains to pinpoint the origin of their seizures. The researchers monitored the electrodes to record neuron activity as memories were being formed.

Using a video game featuring a taxi cab, virtual passengers and a cyber-city, the researchers tested whether deep-brain stimulation of the entorhinal cortex or the hippocampus altered recall. Patients played the role of cab drivers who picked up passengers and traveled across town to deliver them to one of six requested shops.

"When we stimulated the nerve fibers in the patients' entorhinal cortex during learning, they later recognized landmarks and navigated the routes more quickly," Fried said. "They even learned to take shortcuts, reflecting improved spatial memory.

"Critically, it was the stimulation at the gateway into the hippocampus — and not the hippocampus itself — that proved effective," he added.

The use of stimulation only during the learning phase suggests that patients need not undergo continuous stimulation to boost their memory, but only when they are trying to learn important information, Fried noted. This may lead the way to neuro-prosthetic devices that can switch on during specific stages of information processing or daily tasks.

Six million Americans and 30 million people worldwide are diagnosed with Alzheimer's disease each year. The progressive disorder is the sixth leading cause of death in the United States and the fifth leading cause of death for those aged 65 and older.

"Losing our ability to remember recent events and form new memories is one of the most dreaded afflictions of the human condition," Fried said. "Our preliminary results provide evidence supporting a possible mechanism for enhancing memory, particularly as people age or suffer from early dementia. At the same time, we studied a small sample of patients, so our results should be interpreted with caution."

Future studies will determine whether deep-brain stimulation can enhance other types of recall, such as verbal and autobiographical memories. No adverse effects of the stimulation were reported by the seven patients.

WATCH VIDEO: New Study-Electric Shocks To Brain Improve Memory

(Source: Alzheimers Weekly & Dementia Weekly, 12 February 2012)

Hope For Early Alzheimer's Test In Spinal Fluid

2012-02-13T23:23:00.000+08:00

New research led by Nottingham University in the UK suggests abnormal levels of seven proteins in spinal fluid could be markers for the early stages of Alzheimer's disease, raising hopes of a test for a disease that is difficult to diagnose at the beginning. The researchers write about their findings in the Journal of Alzheimer's Disease.

Study co-author Dr Kevin Morgan, Professor of Human Genomics and Molecular Genetics at Nottingham, told the press on Tuesday that the findings are "a new lead for improving early diagnosis of Alzheimer's disease".

An early diagnosis of Alzheimer's disease would help people prepare for the future and also enable them to be involved in clinical trials at a much earlier stage of the disease, when treatments are more likely to show positive results, he added.

About 820,000 people in the UK have dementia, of which Alzheimer's disease is the most common form. Dementia often develops slowly and is not always obvious in the early stages. It can be difficult to distinguish from the mild forgetfulness often seen in normal ageing.

Morgan and colleagues compared samples of cerebrospinal fluid (CSF) from 33 people with Alzheimer's disease, 10 people with mild cognitive impairment, and 20 healthy older people. Mild cognitive impairment is a condition where people have problems with thinking and memory but not to an extent that it interferes with everyday life.

They compiled profiles of the proteins in each sample and then compared them with each other to see if they could find something distinctive in the samples from people with Alzheimer's disease.

The results showed that the samples from people with Alzheimer's diseases tended to have higher levels of four proteins, and lower levels of three other proteins.

A protein called SPARCL1 proved to be the strongest predictor for Alzheimer's. When the researchers tested the samples using only this protein, they could tell whether a person had Alzheimer's disease to an accuracy of 65%.

This accuracy went up to 95% when they tested for abnormal levels of all seven proteins.

The researchers repeated the tests with a new set of CSF samples from 32 healthy people and 30 people with Alzheimer's disease. This time, when they tested for all seven proteins, the accuracy was 85%.

The team now plans to use their findings to develop a blood test for an early diagnosis of Alzheimer's disease.

Morgan said:

"It will also be important to investigate what causes these specific proteins to change as Alzheimer's develops."

By understanding the underlying changes in the biochemistry of Alzheimer's, we have a better chance of developing new treatments, he said, adding that:

"Dementia can only be defeated through research, and I hope these findings could take us a step closer to that goal."

Dr Marie Janson, Director of Development at Alzheimer's Research UK, who part-funded the study, said the findings have "opened up a new avenue for research".

She emphasized how difficult it is to diagnose Alzheimer's, as memory problems can be symptomatic of various conditions.

"This study has the potential to help create a vital tool for doctors to identify patients that need further investigation - but these results must now be followed up in order to achieve that goal," she added.

(Source: Medical News Today, 12 February 2012)

Treat Sleep Apnea – Prevent Vascular Dementia

2012-02-13T06:49:00.002+08:00

A new study links Sleep Apnea to strokes and vascular dementia. Early treatment of Sleep Apnea can protect you from these vascular events.

Study Highlights:
- Sleep apnea is common in people with silent strokes and small lesions in the brain. This vascular damage often evolves into vascular dementia.
- Having more than five sleep apnea episodes per night was associated with silent strokes.
- Early treatment of sleep apnea may help reduce risk of silent strokes in these patients.

People with severe sleep apnea may have an increased risk of silent strokes and small lesions in the brain, which are common foundations of vascular dementia.

The research came out of a small study presented at the American Stroke Association’s International Stroke Conference 2012.

The researchers found:
- Ninety-one percent (51 of 56) of the patients who had a stroke had sleep apnea and were more likely to have silent strokes and white matter lesions that increased risk of disability at hospital discharge.
- Having more than five sleep apnea episodes per night was associated with silent strokes.
- More than one-third of patients with white matter lesions had severe sleep apnea and more than 50 percent of silent stroke patients had sleep apnea.
- Even though men were more likely to have silent infarcts, correlations between sleep apnea and silent infarcts remained the same after adjustment for such gender differences.

As the strokes, infarcts and lesions accumulate, the vascular damage to the brain increases. If left unchecked, too much damage cascades into vascular dementia.
Jessica Kepplinger, M.D., is the study’s lead researcher and stroke fellow in the Dresden University Stroke Center’s Department of Neurology at the University of Technology in Dresden, Germany. Dr. Kepplinger said,

"We found a surprisingly high frequency of sleep apnea in patients with stroke that underlines its clinical relevance as a stroke risk factor."
"Sleep apnea is widely unrecognized and still neglected. Patients who had severe sleep apnea were more likely to have silent strokes and the severity of sleep apnea increased the risk of being disabled at hospital discharge."

The patients — average 67 years old, white and 54% women — underwent overnight in-hospital testing for sleep apnea.

MRI and CT scans were used to check for silent strokes and white matter lesions. Neuroradiologists were blinded to the sleep study findings and outcome.

Researchers suggested sleep apnea should be treated the same as other vascular risk factors such as high blood pressure.

Kepplinger said, "Demographic characteristics in our study are comparable to western European populations, but our findings may not be entirely generalizable to other populations with diverse ethnicities such as in the U.S."

The researchers plan more studies on sleep apnea, particularly in high-risk patients with silent strokes and white matter lesions, to determine the impact of non-invasive ventilation and on short-term clinical outcome, researchers said.

WATCH VIDEO -> Preventative Tips-Treat Sleep Apnea To Prevent Vascular Dementia

More information on:

1. Sleep Apnea Ages Your Brain

2. Is Sleep Apnea Connected to Dementia?

3. Sleep Related Breathing Disorders

(Source: Alzheimer's Weekly and Dementia Weekly News, 12 February 2012)

Research Update : In Mice, Cancer Drug Reduces Beta-Amyloid and Helps Memory

2012-02-13T04:14:00.000+08:00

(Source: Alzheimer's Association Research Update, 10 February 2012)

A report published online by Science Express on Feb. 9, 2012, describes a research study in mouse models of Alzheimer's disease of an FDA-approved cancer therapy called bexarotene. The researchers believe that drug will enhance clearance of an abnormal protein associated with Alzheimer's (beta amyloid protein) from the brain by increasing levels of another protein, known as ApoE. The scientists found that the orally-administered drug rapidly lowered levels of soluble beta amyloid and amyloid plaques in both young and older test animals, and also improved some cognitive and behavioral deficits. This study is exciting because it investigates a possible new approach to treating Alzheimer's disease.

Bexarotene is used to treat cutaneous T-cell lymphoma (CTCL, a type of skin cancer) in people whose disease could not be treated successfully with at least one other medication.

This study, while very interesting, is also very preliminary. Mouse models of Alzheimer's are limited in how closely they represent human Alzheimer's. We are still far away from knowing if this has potential as a therapy for people with Alzheimer's. However, it is intriguing preliminary research that deserves further study.

People with Alzheimer's and their caregivers should not ask their doctor for this drug to treat Alzheimer's disease. That said, investigating an already FDA-reviewed and -approved therapy may mean that the drug development process takes a somewhat shorter time because the drug has already been tested in people. There is still a great deal to learn. For example, without trials in people with Alzheimer's, we know nothing yet about dose levels or how this compound may interact with approved Alzheimer's drugs.

To learn more, following is a report from the Washington Post on 10 February 2012

Cancer Drug Shows Promise In Mouse Alzheimer’s Study

Mice in the early stage of Alzheimer’s disease had some of their brain abnormalities reversed and their declining mental function restored when they were given low doses of a rarely used cancer drug.

The drug, bexarotene, stimulated the removal of beta-amyloid, a substance whose accumulation in the brain appears to be the main cause of Alzheimer’s dementia. After treatment, the animals fared better in tests of memory and social behavior, according to a study published online Thursday by the journal Science.

The findings were dramatic, but their relevance to people with Alzheimer’s disease is unknown. But because the drug is already approved for human use, finding out may be easier than if the drug were an entirely new chemical compound.

“It has to work in humans like it works in mice or we can pick up and go home,” said Gary E. Landreth, a neuroscientist at Case Western Reserve University School of Medicine, who headed the experiment.

A study of bexarotene’s effects in normal brains will start in a few months. Clinical trials in people with early Alzheimer’s — or at high risk for the disease for genetic reasons — will take years. If the drug’s effect in human brains turns out to be different, it may never move on to be tested in Alzheimer’s patients.

Nevertheless, the researchers think speed is important, as they fear that people might start using the drug before it is fully evaluated. A few days ago, Landreth got a call from a physician in another city. A person who had heard of the drug through the grapevine had asked for a prescription for bexarotene.

“We’ve got to work fast, and we have got to be right. We can’t screw this up,” Landreth said.

About 5.4 million Americans have Alzheimer’s disease, which is the leading cause of dementia. About 5 percent of people in their late 60s suffer from it, and possibly half of people in their late 80s. By 2050, 1 in 85 people worldwide will have the disease, according to one estimate.

Bexarotene is in the retinoid family of compounds, which are all chemically related to Vitamin A. Retinoids affect cell division and growth, immunity and other essential biological functions.

Sold under the trade name Targretin, bexarotene is approved by the Food and Drug Administration as a treatment for cutaneous T-cell lymphoma, a disease diagnosed in about 3,000 Americans a year. It is an “orphan drug,” a designation that gives drug companies an incentive to develop medicines for rare diseases. Orphan drugs stay under patent protection longer than regular drugs. It has been tried against other forms of cancer, without impressive results.

Numerous “candidate” Alzheimer’s drugs, which looked promising in lab studies, have washed out in recent years.

Last month, Pfizer and a smaller partner announced that they were abandoning a drug called Dimebon as a possible Alzheimer’s drug after it failed to show benefit in a clinical trial. In 2010, Lilly halted development of a different compound, semagacestat. At the Alzheimer’s Association, an advocacy organization, the new study’s results were greeted with that history noted.

“This is an early study and it was in mice,” said Maria C. Carrillo, the organization’s director of scientific relations. “We need to be cautiously optimistic and pursue this lead as we would any other.” She added that what makes “this an exciting study is that it involves a repurposed drug.”

The Case Western experiments were conducted by Paige E. Cramer, a graduate student in Landreth’s lab. The mice used had genetic defects that allowed beta-amyloid to accumulate in their brains, which in turn changed their behavior. The animals, however, are an imperfect model for the human disease. They don’t lose brain cells after beta-amyloid accumulates as people with Alzheimer’s do. (In people, dementia can begin even before cells die, as beta-amyloid disrupts the normal firing of nerve cells.)

Bexarotene spurred the production of “apoE,” a protein that breaks down beta-amyloid molecules floating in the watery fluid between brain cells. Beta-amyloid levels fell by 25 percent within a few days of a single dose. The drug also stimulated housekeeping cells called microglia to consume plaques of solidified beta-amyloid.

While the density of plaques fell by 75 percent over a few weeks, eventually they reaccumulated. Curiously, however, the animals’ behavior didn’t regress to its former state.

“It appears that the measurable activity of the brain is not affected by the presence of the plaques. I think that is a really interesting finding that will stimulate a lot of new science,” Landreth said.

The behavioral tests involved an animal’s ability to remember a cage in which it had gotten a shock, to find a submerged platform in a pool of water, to identify a smell and to build a nest. After treatment with the drug, all those activities returned to normal.

Several physicians with patients taking bexarotene say they’ve never noticed mental improvement from the drug, although they have few, if any, demented patients under their care.

“I have treated over 500 patients with cutaneous T-cell lymphoma in studies and in practice with bexarotene and have not heard any beneficial effect on the brain or cognitive function,” Madeleine Duvic of M.D. Anderson Cancer Center in Houston wrote in an e-mail.

“We really didn’t see anything like this,” said Heather Wakelee, a cancer researcher at Stanford University. She noted, however, that demented people were excluded from studies of bexarotene in advanced cancer.

ALZHEIMER'S ASSOCIATION INVOLVEMENT

Six months before this research was published, the Alzheimer's Association awarded the senior scientist on this article, Gary Landreth of Case Western Reserve University, Cleveland, our prestigious Zenith Award in 2011 for research that will follow on from this study to investigate this drug and how and why it works in this way, perhaps setting the stage for trials in people.

We need to create more treatment targets for Alzheimer's disease and the only way to do that is with more research, especially basic research into the causes and progression of the disease. The Alzheimer's Association commendsthe Obama Administration for dedicating new resources in the fight against Alzheimer's in a uniquely challenging fiscal year in advance of the first ever National Alzheimer's Plan. The Alzheimer's Association will continue to support the process underway to develop the first National Alzheimer's Plan led by Health and Human Services Secretary Kathleen Sebelius. This will help ensure the nation is equipped to overcome Alzheimer's the public health crisis of this century and meet the goal set forth by the Administration to prevent and effectively treat Alzheimer's disease by 2025.

Metals Could Be A Potential Target In Fighting Alazheimer's

2012-02-02T15:06:00.001+08:00

One of the many theories explaining Alzheimer's disease is that some of the harm is caused by toxic metals accumulating in brain. Now a new study lends more credibility to the toxic metal theory.

Research into how iron, copper, zinc and other metals work in the brain may help unlock some of the secrets of degenerative diseases like Alzheimer's and Parkinson's.

Iron and copper appear to accumulate beyond normal levels in the brains of people with these diseases, and a new, Australian study published Sunday shows reducing excess iron in the brain can alleviate Alzheimer's-like symptoms - at least in mice.

A genetic mutation related to regulating iron is linked to ALS, or Lou Gehrig's disease. Zinc, on the other hand, appears to impair memory if its levels get too low or if it gets into a brain region where it doesn't belong, as it can with traumatic brain injury.

Research into the complicated, invisible roles these metals play in brain diseases has lagged behind study of the more-visible proteins that are damaged or clump together in the brains of Alzheimer's and Parkinson's sufferers. But better understanding metals' role in the brain could help shed light on a range of medical conditions and might offer a new route for developing treatments, scientists say.

"The field is coming around to the idea of the cause of Alzheimer's being multifactorial," and disturbed metal regulation could be one of those factors, says Ralph Nixon, Chairman of the Alzheimer Association's Medical and Scientific Advisory Council and Director of the Silberstein Alzheimer's Institute at New York University.

Tiny metal ions - charged particles of the elements - serve several essential functions in the body, including facilitating chemical reactions to generate energy and preserving the structure of proteins. Strict checks and balances in a healthy body keep metal levels within a tight range.

But the biological changes that come with disease and aging - as opposed to poisoning from outside sources like food, supplements or metal pans - can knock levels of these metals out of whack in the brain.

Iron, for instance, is a "double-edged sword" because it interacts with oxygen to help the body generate energy, but also can produce free radicals, highly reactive molecules that can cause cell damage, says James Connor, professor and vice chairman of neurosurgery at Penn State University in Hershey.

If the body has too little iron, such as with anemia, the body doesn't generate enough energy to sustain important functions. But an overabundance of iron accumulated in the brain is toxic. Significantly higher accumulations of metal have been observed in the brains of people with Parkinson's and Alzheimer's disease than in healthy people of the same age, says Ashley Bush, a Professor of Pathology at the University of Melbourne.

The new study, conducted by Dr. Bush and colleagues and published in the Journal Nature Medicine, examined the amount of iron in the brains of mice that were bred unable to produce the tau protein, which helps stabilize the structure of neurons. Tau damage is associated with Alzheimer's and Parkinson's.

As the mice aged, they suffered symptoms similar to people with both diseases, including impaired short-term memory, and also exhibited an accumulation of iron in their brains. When the researchers gave them a drug removing excess iron, the symptoms reversed. This means normally functioning tau is necessary for removing iron in the brain, Dr. Bush says. The finding bolsters previous research showing that bringing down iron may be a path to new treatments.

"An accumulation of iron in neurons seems to be a final end-stage event in neurodegeneration, whether it be Alzheimer's or Parkinson's, [or] any [condition] related to tau abnormalities," says Dr. Bush, who is also a fellow at the university's Mental Health Research Institute.

Other proteins affected in Alzheimer's also play a role in metal regulation. The amyloid precursor protein is important in helping export iron from the brain, according to work published in the Journal Cell in 2010. Presenilin, another protein that aids in metal uptake, is also disturbed in diseased brains, according to a study published in Journal of Biological Chemistry last year.

Similar findings link copper accumulation and brain disease, though not as much research has been conducted as with iron, scientists say.

In addition to iron accrual, lower-than-normal levels of zinc have been found in patients with Alzheimer's and Parkinson's disease, according to work by George Brewer, an emeritus professor at the University of Michigan, and Edward Fitzgerald at the University at Albany-SUNY, published last year in the American Journal of Alzheimer's Disease and Other Dementias. Dr. Brewer now is a consultant to Adeona Pharmaceuticals Inc., based in Ann Arbor, Mich., which is developing a zinc-based treatment for Alzheimer's, he says.

Besides Adeona, a handful of other biotechnology companies have also been testing experimental metal-lowering drugs for treatment of Alzheimer's or Parkinson's. But developing such drugs is tricky because it is hard to target metals in specific parts of the brain. Simply lowering or increasing the amount overall in the body may not be beneficial, researchers say.

Metals may play a vital role in other brain conditions.

Stephen Lippard, a Chemistry Professor at the Massachusetts Institute of Technology, and colleagues from Duke University and the University of Toronto, found zinc helps neurons communicate in the hippocampus, a brain region involved in learning and memory. Disturbing this interaction, or ushering zinc into a brain region where it doesn't belong, could affect memory formation and the occurrence of epileptic seizures, says Dr. Lippard, who studies the role of metal ions in biology, neuroscience, and medicine. Their work was published in September in Neuron.

"It's important that the medical community continue to be alerted to the connection between metal ions and neurological disease," says Dr. Lippard.

Dr. Connor and his Penn State team have shown that patients with ALS have a higher rate of mutation in a gene, HFE, that regulates iron absorption. Carriers of the mutation have higher levels of iron in the brain and a fourfold increase in risk of ALS, according to a 2004 study published in the Journal of Neurological Sciences.

They have also been trying to figure out why the patients with multiple sclerosis lose the protective coating, called myelin, surrounding their axons, the part of the nerve cell that conducts electrical impulses. The cells responsible for making the myelin have elevated iron, making them more vulnerable to damage and death, says Dr. Connor.

Metals, Positive and Negative

Several metals play vital roles in the human body, but diseases can disturb their balance, causing harm.

Iron

Normal function: Involved in oxygen transport; needed to make energy for cells.

In the brain: Excess levels of iron are linked to Alzheimer's and Parkinson's diseases. Proteins and mutations related to iron delivery or absorption appear to be connected to Lou Gehrig's disease and multiple sclerosis.

Copper

Normal function: Helps transport oxygen, often works in tandem with iron.

In the brain: Wilson disease stops the body from getting rid of copper, which can cause speech problems, tremors and muscle stiffness. Disruption in copper regulation causes Menkes disease, which leads to abnormally low copper levels.

Zinc

Normal function: Helps make DNA and RNA, regulates cell death, and plays a role in short-term memory and learning.

In the brain: Low levels or the presence of the metal in areas of the brain where it isn't normally found are thought to impair memory.

Watch Video -> Do Toxic Metals In The Brain Cause Alzheimer's

(Source: WSJ (The Wall Street Journal), 31 January 2012, By SHIRLEY S. WANG)

(SAT) 11FEB12 Talk "Caring with Love" Organized By ADFM KL-PJ Caregivers Support Group

2012-01-11T15:57:00.003+08:00

Dear Caregivers/Members,

ADFM KL-PJ ALZHEIMER'S CAREGIVERS SUPPORT GROUP

MONTHLY GATHERING & TALK

“CARING WITH LOVE”

SATURDAY, 11 FEBRUARY 2012 AT 2:00PM

ADFM PJ DAYCARE CEMTRE

(No. 6, Lorong 11/8E,Section 11, 46000 PJ)

BY SPEAKER, MADAM LEONG SIK WAI

Program:
2:00pm : Registration of Attendance
2:30pm : Welcome address by the Chairperson
2:40pm : “Caring with Love” by Guest Speaker, Mdm Leong Sik Wai,
3:40pm : Sharing and Q & A Session
4:20pm : Refreshments

The Objective:

· To reinforce on the patient’s feeling and caregiver’s coping skill.

· How caregivers can better understand the physical, emotional, and mental changes of their patients.

· Caregiver’s feeling - understand own feeling, be able to cope with patient’s condition/changes.

· Learn the techniques - “LOVE” (how to love ), Emotion Freedom Technique.

The Speaker:

Mdm Leong Sik Wai is currently a Nutrionist with Merck, a Pharmaceutical Company, a Caregiver for her late Dad, Speaker for the Malaysian Healthy Aging Society’s Caregivers Workshop on “Caring with Love” and Volunteer with the Tzu Chi Charity Foundation. She obtained her BSc.(Hons) Nutrition from UKM.

To Register, submit "Registration Form" and Email: jenny@adfm.org.my OR Fax: 03 - 7960 8482.

Further enquiries, call Jenny at ADFM 03-7956 2008/7958 3008 / SMS 016-608 2513 or Email: jenny@adfm.org.my

JOIN ADFM NATIONAL ALZHEIMER'S CAREGIVERS NETWORK

The National Platform for The Caregivers Community

From: ADFM KL-PJ Caregivers Support Group

January 2012

Advice to Keep Dementia at Bay

2012-01-11T03:36:00.001+08:00

Recently, researchers looking into cognitive decline and dementia have made encouraging findings. Although it was believed that the adult brain could not develop new neurons (or brain cells), scientists have learned in the past decade or so that the human brain is pliable and adaptive. The brain can actually add new neurons even late in life and continually form new connections among existing neurons -- a phenomenon known as neuroplasticity.

This means that while an aging brain may have signs of damage, it can often compensate for them, at least initially. And engaging in mentally stimulating activities like reading, taking a class or playing board games is one way to bolster this process.

This compensation process depends on your "cognitive reserve," the extra, perhaps unused, amount of cognitive ability that can make up for the loss of brain functioning when your brain shows signs of dementia due to the death of cells and their replacement by beta-amyloid plaques. Genetics, early childhood stimulation and education level can influence cognitive reserve but are essentially immutable once you're an adult.

Fortunately, studies have found that you can also increase your cognitive reserve and delay the onset of dementia through a variety of intellectually stimulating leisure activities in middle and later life.

A study in the journal Neurology, for example, found that among 101 people who eventually developed dementia, those who frequently participated in one or more activities, such as reading, writing, doing crossword puzzles, playing card or board games, having group discussions or playing music experienced memory decline more than one year later than those who participated in these activities less often. These pursuits built cognitive reserve and delayed dementia as much as a higher education level did.

It's worth noting that researchers have discovered that watching television is a passive activity that doesn't really stimulate the mind at all; on the contrary, watching television is associated with an increased risk of cognitive decline. One study found that TV watchers were 10 percent more likely than nonwatchers to experience cognitive impairments over a five-year period. A possible explanation: Time spent in front of the TV means less time for the mental, social and physical activities that can help delay dementia.

(Source: John Hopkins Health Alert, 9 January 2012)

Medical News / Treatment Articles: Drugs In Dementia - Everything You Wanted to Know

2012-01-06T20:05:00.000+08:00

VIDEO - Watch Dr Frank Molnar's brilliant presentation on "Drugs in Dementia - The Good, The Bad, The Ugly" at the October 2011 Alzheimer Society of Ottawa and Renfrew County education seminar. Learn the best use of Namenda, Antipsychotics and Cholinsterase Inhibitors like Aricept. See what distinguishes Alzheimer's, Frontotemporal Lobar, Lewy body, Parkinson's, PPA, Semantic and Vascular Dementias. Understand the side-effects and interactions of antibiotic, antidepressant, heart, narcotic and other medications in dementia. Whether patient, caregiver or neurologist, you'll get many answers.

Recommend to read:

1. Charts Comparing Medications to Treat Alzheimer's Disease and Related Dementias

This brief summary does not include all information important for patient use and should not be used as a substitute for professional medical advice. Consult the prescribing doctor and read the package insert before using these or any other medications or supplements. Drugs are listed in alphabetical order.

TECHNICAL FACTS

BRAND NAME	GENERIC (Int'l) NAME	STAGE OF ILLNESS	DRUG TYPE	HOW IT WORKS	LOGO
ARICEPT®	donepezil	Mild to moderate & Moderate to severe	Cholinesterase inhibitor	Prevents the breakdown of acetylcholine in the brain.
EXELON®	rivastigmine	Mild to moderate	Cholinesterase inhibitor	Prevents the breakdown of acetylcholine and butyrylcholine (a brain chemical similar to acetylcholine) in the brain.
NAMENDA®	memantine	Moderate to severe	N-methyl D-aspartate (NMDA) antagonist	Blocks the toxic effects associated with excess glutamate and regulates glutamate activation.
RAZADYNE®	galantamine	Mild to moderate	Cholinesterase inhibitor	Prevents the breakdown of acetylcholine and stimulates nicotinic receptors to release more acetylcholine in the brain.

PRESCRIPTION FACTS

BRAND NAME	MANUFACTURER’S RECOMMENDED DOSAGE	GENERIC VERSION?	FORMAT	COMMON SIDE EFFECTS	MORE INFORMATION
ARICEPT®	. Initial dose: 5-mg tablet once a day . May increase dose to 10 mg/day after 4-6 weeks if well tolerated.	No	Tablet	Nausea, vomiting, diarrhea	Visit www.fda.gov/cder. Click on “Drugs@FDA,” search for ARICEPT®, and click on drug-name links to see “Label Information.
EXELON®	. Capsule: Initial dose of 3 mg/day (1.5 mg twice a day). . May increase dose to 6 mg/day (3 mg twice a day), 9 mg (4.5 mg twice a day), and 12 mg/day (6 mg twice a day) at minimum 2-week intervals if well tolerated. . Patch: Initial dose of 4.6 mg once a day; may increase to 9.5 mg once a day after minimum of 4 weeks if well tolerated. . Also available as oral solution; same dosage as capsule.	No	Capsule Patch Oral Solution	Nausea, vomiting, diarrhea, weight loss, loss of appetite, muscle weakness	Visit www.fda.gov/cder. Click on “Drugs@FDA,” search for EXELON®, and click on drug-name links to see “Label Information.”
NAMENDA®	. Initial dose: 5-mg tablet once a day. . May increase dose to 10 mg/day (5 mg twice a day), 15 mg/day (5 mg and 10 mg as separate doses), and 20 mg/day (10 mg twice a day) at minimum 1-week intervals if well tolerated. . Also available as oral solution; same dosage as above.	No	Tablet Oral Solution	Dizziness, headache, constipation, confusion	Visit www.namenda.com. Click on “Prescribing Information” to see the drug label.
RAZADYNE®	. Tablet: Initial dose of 8 mg/day (4 mg twice a day). . May increase dose to 16 mg/day (8 mg twice a day) and 24 mg/day (12 mg twice a day) at minimum 4-week intervals if well tolerated. . Extended-release capsule: Same dosage as above but taken once a day. . Also available as oral solution; same dosage as above.	Yes	Tablet Once-A-Day Extended Release Capsule Oral Solution	Nausea, vomiting, diarrhea, weight loss, loss of appetite	Visit www.razadyneer.com. Click on “Important Safety Information” to see links to prescribing information.

2. Introduction To Medications

Learn about the 4 prescription drugs currently approved by the U.S. Food and Drug Administration (FDA) to treat people who have been diagnosed with Alzheimer’s disease (AD). Treating the symptoms of AD can provide patients with comfort, dignity, and independence for a longer period of time and can encourage and assist their caregivers as well.

It is important to understand that none of these medications stops the disease itself.

Treatment for Mild to Moderate AD

Medications called cholinesterase inhibitors are prescribed for mild to moderate AD. These drugs may help delay or prevent symptoms from becoming worse for a limited time and may help control some behavioral symptoms. The medications include: Razadyne® (galantamine, formerly known as Reminyl® and now available as a generic drug), Exelon® (rivastigmine), and Aricept® (donepezil). Another drug, Cognex® (tacrine), was the first approved cholinesterase inhibitor but is rarely prescribed today due to safety concerns.

Scientists do not yet fully understand how cholinesterase inhibitors work to treat AD, but research indicates that they prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking. As AD progresses, the brain produces less and less acetylcholine; therefore, cholinesterase inhibitors may eventually lose their effect.

No published study directly compares these drugs. Because they work in a similar way, switching from one of these drugs to another probably will not produce significantly different results. However, an AD patient may respond better to one drug than another.

Treatment for Moderate to Severe AD

A medication known as Namenda® (memantine), an N-methyl D-aspartate (NMDA) antagonist, is prescribed to treat moderate to severe AD. This drug’s main effect is to delay progression of some of the symptoms of moderate to severe AD. It may allow patients to maintain certain daily functions a little longer than they would without the medication. For example, Namenda® may help a patient in the later stages of AD maintain his or her ability to use the bathroom independently for several more months, a benefit for both patients and caregivers.

Namenda® is believed to work by regulating glutamate, an important brain chemical. When produced in excessive amounts, glutamate may lead to brain cell death. Because NMDA antagonists work very differently from cholinesterase inhibitors, the two types of drugs can be prescribed in combination.

The FDA has also approved Aricept® for the treatment of moderate to severe AD.

Dosage and Side Effects

Doctors usually start patients at low drug doses and gradually increase the dosage based on how well a patient tolerates the drug. There is some evidence that certain patients may benefit from higher doses of the cholinesterase inhibitors. However, the higher the dose, the more likely are side effects. The recommended effective dosages of drugs prescribed to treat the symptoms of AD and the drugs’ possible side effects are summarized in the table (see below).

Patients should be monitored when a drug is started. Report any unusual symptoms to the prescribing doctor right away. It is important to follow the doctor’s instructions when taking any medication, including vitamins and herbal supplements. Also, let the doctor know before adding or changing any medications.

3. How Do Alzheimer's Medications Differ?

Which Alzheimer's medications are best? To help answer this question, the ACP/AAFP Committee issued guidelines on the five available medications for Alzheimer's.

An American College of Physicians (ACP) and American Academy of Family Physicians (AAFP) committee issued a clarifying guideline on drug treatment of dementia. Their advice? When trying to decide which medicine is best for a person, the most important considerations are:

Side effects

Ease of Use

Cost

There's no proof that any one of the five drugs available in the United States to treat dementia in general, and Alzheimer's in particular, is more effective than the others.

The committee reviewed published studies for outcomes such as cognition, global function, behavior/mood, and quality of life/activities of daily living. They found only limited high-quality scientific evidence of the effectiveness of the drugs and therefore developed the following cautious recommendations:

· The decision to use approved drugs for dementia should be based on an individualized patient assessment.

· The choice of drugs should be based on tolerability, adverse effect profile,ease of use, and cost.

· There's an urgent need for more clinical research to improve knowledge about the clinical effectiveness of drugs used to treat dementia.

The committee recommended the following kinds of research:

· Evaluate the effectiveness of drug therapy for dementia and assess whether treatments affect key outcomes, such as institutionalization.

· Evaluate the appropriate duration of therapy.

· Head-to-head testing of drugs.

· Test drugs in combination therapy.

The guideline was published in the Annals of Internal Medicine.

Currently, there are five FDA-approved drugs for treatment of dementia. These include four acetylcholinesterase inhibitors - donepezil (Aricept®), galantamine (Razadyne®, Reminyl), rivastigmine (Exelon®), and tacrine - and one neuropeptide-modifying agent - memantine (Namenda®).

While these drugs may improve symptoms or slow disease progression, they don't cure dementia or repair brain damage.

"Doctors, patients and family caregivers desperately want information on how to treat this disease," Dr. Amir Qaseem, senior medical associate in the ACP's Clinical Programs and Quality of Care Department, said in a prepared statement.

"More research is warranted, because the available evidence concerning these pharmaceuticals' effects on quality of life is mixed, and the clinical significance of many of the findings is questionable," Dr. Kenneth G. Schellhase, an AAFP representative on the committee, said in a prepared statement. "In addition, the duration of existing trials was usually less than one year, providing insufficient information to determine the optimal length of treatment, and few trials compare one drug directly with another."

Most existing studies of the five approved dementia drugs focused on statistical significance of changes, but clinically important improvement is what matters to patients, caregivers and doctors, the committee noted. Many studies measuring clinical improvements are currently in progress throughout the world.

4. Behavioral Benefits of Alzheimer's Medications

People with Alzheimer's and other dementias often take medications called cholinesterase inhibitors.

Medical research has demonstrated they are also a safe alternative to antipsychotics for the behavioral and psychological symptoms of dementia.

This is according to a study that appears in the December 2008 edition of Clinical Interventions in Aging.

Currently, the main cholinesterase inhibitors that are offered for Alzheimer's and other dementias are:

Brand Name	Generic Name
Aricept	donepezil HCL
Exelon	rivastigmine
Razadyne®	galantamine HBr

Investigators from the Indiana University School of Medicine, the Regenstrief Institute and Wishard Health Services reviewed nine randomized, double-blind, placebo-controlled clinical trials evaluating the effectiveness of three popular cholinesterase inhibitors in managing behavioral and psychological symptoms displayed by patients with Alzheimer's disease.

The researchers report that the trial results indicate cholinesterase inhibitors led to a statistically significant reduction in behavioral and psychological symptoms such as aggression, wandering or paranoia when using the same dosage as administered for improving cognitive impairment.

Nine out of 10 Alzheimer's disease patients display behavioral and psychological symptoms of their disease. The review of the clinical trials revealed that cholinesterase inhibitors are safe, producing no major side effects.

"There is a need for safe alternatives to the anti-psychotic drugs currently used to manage the behavioral and psychological symptoms of Alzheimer's disease. The results of the studies we analyzed are encouraging and suggestive that cholinesterase inhibitors are safe and effective alternatives. However, they are underutilized and typically prescribed for less than three months and for less than 10 percent of patients with Alzheimer's disease. Our findings might provide clinicians with useful data to justify the appropriate use of these medications," said Malaz Boustani, M.D., corresponding author of the Clinical Interventions in Aging paper. Dr. Boustani is assistant professor of medicine at the IU School of Medicine, a Regenstrief Institute research scientist, a research investigator with the IU Center for Aging Research, and chief research officer of the Indianapolis Discovery Network for Dementia.

In Alzheimer's disease there is a decrease in acetylcholine, a chemical in the brain that assists memory, thought and judgment. Cholinesterase inhibitors raise acetylcholine levels. Increased concentrations of acetylcholine in the brain leads to increased communication between nerve cells and may improve or stabilize the symptoms of Alzheimer's disease in the early and moderate stages of progression.

Noll Campbell, PharmD, a clinical pharmacy specialist in geriatric psychiatry with Wishard Health Services and corresponding author of the paper, said that, "This class of medications has already been approved by the Food and Drug Administration to manage symptoms of Alzheimer's-type dementia, although their potential benefits on behavioral symptoms are not frequently identified by many prescribers. Clinical trials of cholinesterase inhibitors have shown benefits in several domains of cognitive function as well as behavioral symptoms associated with dementia, and may improve the management of behavioral problems while reducing the use of more harmful medications that are needed to control behaviors."

Dr. Boustani noted that the vast majority of busy primary care physicians, the doctors who see the majority of patients with Alzheimer's disease, are unaware of the details of the studies analyzed in the Clinical Interventions in Aging paper and he hopes that this new paper, which reviewed the studies, will encourage them to prescribe cholinesterase inhibitors, with its benefits for both cognition and behavior symptoms to their Alzheimer's disease patients.

5. Moderate Your Medications

Almost 190,000 Australians have dementia and as Australia's population ages, dementia becomes a bigger challenge for doctors, their patients and carers.

According to the National Prescribing Service Limited (NPS), there are limited benefits to using cholinesterase inhibitors and memantine in the treatment of patients with dementia drug therapy.

Research indicates that the benefits of cholinesterase inhibitors and memantine are small, some people will not respond and adverse effects are common, says NPS clinical expert, Education and Quality Assurance Program Manager, Ms Judith Mackson.

Because the response rate is low and the effects of cholinesterase inhibitors and memantine are small, if these medicines are to be used, it is imperative that they are monitored in order to objectively assess their effectiveness for the patient.

Antipsychotics have a very limited role in some of the challenging behaviours of dementia and the risk of cerebrovascular events and all-cause mortality increases. Consequentially if there are no clear beneficial effects, a trial withdrawal should be attempted because for many patients symptoms will NOT worsen on withdrawal.

A planned, regular and also opportunistic approach to reviewing medications is recommended not only for people with Alzheimer's disease, but all older people using medicines, Ms. Mackson said.

She says health professionals need to encourage the use of non-pharmacological strategies at all stages of dementia. We know that non-pharmacological strategies can help promote and maintain independence, cognitive function and manage the behavioural and psychological symptoms of dementia.

Carers may see medication as the only option, so they will need support and information to help manage their expectations on the effectiveness of medication, she said. "Appropriate counseling for carers from health professionals on the limited benefits of drug therapy is key to best practice. In addition, carers may need information about the process of withdrawal if there are no clear beneficial effects of the medication."

To learn more about how to make informed decisions when working with patients with dementia, the new NPS education program, Treating the symptoms of dementia may be of interest. To obtain a copy,or to find out about the education program, visit the NPS website www.nps.org.au.

(Source: Alzheimer's & Dementia Weekly, 2 January 2012)

Prevention Tip - Exercise Against Alzheimer's ...

2012-01-03T12:28:00.004+08:00

What can we do to fight dementia? There is ever-growing evidence that exercise is both highly therapeutic and powerfully protective.

1. Watch this Video "Staying Active may deter Alzheimer's" for insights to help get your new year in motion.

2. BRAIN CONNECTIVITY BOOSTED BY DIFFERENT "ALZHEIMER'S WALK"

A group of “professional couch potatoes,” as one researcher described them, has proven that even moderate exercise - in this case walking at one’s own pace for 40 minutes three times a week - can enhance the connectivity of important brain circuits, combat declines in brain function associated with aging and increase performance on cognitive tasks.

The study, in Frontiers in Aging Neuroscience, followed 65 adults, aged 59 to 80, who joined a walking group or stretching and toning group for a year. All of the participants were sedentary before the study, reporting less than two episodes of physical activity lasting 30 minutes or more in the previous six months. The researchers also measured brain activity in 32 younger (18- to 35-year-old) adults.

Rather than focusing on specific brain structures, the study looked at activity in brain regions that function together as networks.

“Almost nothing in the brain gets done by one area - it’s more of a circuit,” said University of Illinois psychology professor and Beckman Institute Director Art Kramer, who led the study with kinesiology and community health professor Edward McAuley and doctoral student Michelle Voss. “These networks can become more or less connected. In general, as we get older, they become less connected, so we were interested in the effects of fitness on connectivity of brain networks that show the most dysfunction with age.”

Neuroscientists have identified several distinct brain circuits. Perhaps the most intriguing is the default mode network (DMN), which dominates brain activity when a person is least engaged with the outside world - either passively observing something or simply daydreaming.

Previous studies found that a loss of coordination in the DMN is a common symptom of aging and in extreme cases can be a marker of disease, Voss said.

“For example, people with Alzheimer’s disease tend to have less activity in the default mode network and they tend to have less connectivity,” she said. Low connectivity means that the different parts of the circuit are not operating in sync. Like poorly trained athletes on a rowing team, the brain regions that make up the circuit lack coordination and so do not function at optimal efficiency or speed, Voss said.

In a healthy young brain, activity in the DMN quickly diminishes when a person engages in an activity that requires focus on the external environment. Older people, people with Alzheimer’s disease and those who are schizophrenic have more difficulty “down-regulating” the DMN so that other brain networks can come to the fore, Kramer said.

A recent study by Kramer, Voss and their colleagues found that older adults who are more fit tend to have better connectivity in specific regions of the DMN than their sedentary peers. Those with more connectivity in the DMN also tend to be better at planning, prioritizing, strategizing and multi-tasking.

The new study used functional magnetic resonance imaging (fMRI) to determine whether aerobic activity increased connectivity in the DMN or other brain networks. The researchers measured participants’ brain connectivity and performance on cognitive tasks at the beginning of the study, at six months and after a year of either walking or toning and stretching.

At the end of the year, DMN connectivity was significantly improved in the brains of the older walkers, but not in the stretching and toning group, the researchers report.

The walkers also had increased connectivity in parts of another brain circuit (the fronto-executive network, which aids in the performance of complex tasks) and they did significantly better on cognitive tests than their toning and stretching peers.

Previous studies have found that aerobic exercise can enhance the function of specific brain structures, Kramer said. This study shows that even moderate aerobic exercise also improves the coordination of important brain networks.

“The higher the connectivity, the better the performance on some of these cognitive tasks, especially the ones we call executive control tasks - things like planning, scheduling, dealing with ambiguity, working memory and multitasking,” Kramer said. These are the very skills that tend to decline with aging, he said.

3. Video and Article "10 Ways Exercise Fights Dementia"

Exercise is good, but it's hard to do. Get motivated by learning 10 ways it helps your brain prevent & fight dementias such as Alzheimer's.

4. Video and Article "Walking is Best Brain Protector. The Easiest and The Cheapest"

A recent study that shows walking not only protects the brain, but can help improve memory in older adults. Watch Dr. Morgan Sauer from the St. Vincent Longevity Center.

(Source: The Alzheimer's Weekly and Dementia Weekly, 2 January 2012)

iPods Can Help People With Alzheimer's Remember

2011-12-29T14:39:00.004+08:00

It's a diagnosis that we dread, both for our loved ones and ourselves: Alzheimer's disease. Although at first glance, it may seem that the disease has robbed a person of their sense of self, this is not always the case. Not all people with Alzheimer's and other forms of dementia entirely lose their sense of self. The feelings, emotions and memories of experiences that make them who they are may still reside inside of them. It's their ability to access this sense of self that now becomes the challenge.

Scientists at research organizations, such as the Institute for Music and Neurologic Function (IMNF), have been studying the effects of music on the human condition for more than 30 years. And results have been promising. Now, technology is playing a key role in helping people with Alzheimer's disease and other forms of dementia reconnect to their memories and their loved ones, if only for immediate and short periods of time.

As MP3 players such as the iPod have become more mainstream, they are being used as part of music therapy. A new program, called "Well-Tuned: Music Players for Health," is helping people who suffer from Alzheimer's disease ... and it is music to caregivers' ears.

Professionals from IMNF will work with caregivers to develop a play list of music that is emotionally significant to the person with dementia. The play list is customized based on the elder's life experiences, cultural backgrounds and frame of reference. As with lovers who grow sentimental when "their song" is played on the radio, the right music stimulates the personal associations that it is connected with, sparking memory and renewed "presence." It is best to select music that is familiar, enjoyable and meaningful to the elder with dementia.

How iPod music helps Alzheimer's patients with memory

Caregivers can also enhance the impact of the music with meaningful photos of family, friends or by telling family stories and talking about past events. Often, the music can spark memories that were thought to be long gone, or stimulate recognition of a loved one that moments earlier was no more than a blank face. Music may also help a person with dementia transition more easily throughout the day. Playing lively, upbeat music can be used as a stimulus to help motivate an elder to take a walk or participate in an activity. Alternatively, slower, more calming music will help relax an elder when they are agitated or help them wind down as bedtime approaches. The science behind music therapy has to do with the emotional connections we make to music throughout our life and where in the brain those connections live. Music stimulates the areas of the brain that are involved in emotion, association and long-term memory processes for people with Alzheimer's disease and other forms of dementia. As a result, musical selections that are linked to emotions and personal experiences can unlock memories and associations. Senior residential facilities, adult day care centers, and assisted living centers are now using music therapy as part of the residents' routine. For caregivers, seeing the light of recognition in a loved one's eyes is priceless.

(Source: By Dr. Concetta M. Tomaino, Agingcare.com)

How to Plan Meaningful Activities for Someone with Alzheimer's

2011-12-29T12:03:00.005+08:00

A multitude of research studies have come out over the years, touting the benefits of keeping seniors with memory disorders physically and mentally active. But, coming up with activities to keep a person with Alzheimer's busy and engaged with life can be a tricky task for a caregiver.

There are a few things that you should keep in mind when considering various pastimes: First, as your loved one begins to forget who they are, it's all the more important that you remember, and try to present them with meaningful activities that echo their previous interests and talents.

It's also important to remember that, for many people with Alzheimer's and other memory-altering diseases, their desire to accomplish things doesn't vanish. Activities that can give an elderly loved one a sense of accomplishment may help stave off anxiety and depression.

Here are a few examples of easily-modifiable activities that may be good for seniors with Alzheimer's:

1. Stick to Simple Pleasures-Keeping things simple and straightforward is often the best course of action when coming up with activities for people with Alzheimer's. Going to a local park to feed the birds and fish is an easy task that may be very fun for a person with Alzheimer's. You can also take turns reading a favorite book aloud. This can be an easy way to encourage a senior to exercise their mind while giving them the pleasure of reading a beloved book.

2. Listen to Music-Research has shown that listening to music can help a person with Alzheimer's remember events, people, and places from their past. Additionally, music can be a way to get a senior moving through dance or song.

3. Cook and Clean-You can turn mundane, daily tasks into activities that a person with Alzheimer's can help with. Even if they just help with measuring ingredients, having a senior help you cook a family recipe can be a fun way for both of you to spend some time together. An elderly loved one might also be able to help you do things around the house like dusting or folding laundry.

4. Work Up A Sweat-Exercise provides countess benefits to all seniors, regardless of whether or not they have Alzheimer's. Workouts can consist of everything from talking a walk around the block to taking a yoga-for-seniors class.

5. Play A Game-While you probably don't want to start a game of Risk with your elderly loved one, it's possible to make an entertaining, personal game out of things lying around the house. Sorting through old family photos is a good way to help an elderly loved one remember special events and people from their past. You can even turn a routine trip to the grocery store into a scavenger hunt where you and your loved one search for particular items on a list.

6. Volunteer-Devoting time to helping other people can provide immense satisfaction to both you and your elderly loved one. Volunteering can involve something as simple as collecting things like school supplies, toys, canned goods, etc., and taking them to a local shelter or food bank. Seniors who can't leave the house could help by sorting, wrapping, or taking inventory of collected goods.

These activities will require varying levels of patience on the part of the caregiver. A loved one with Alzheimer's will not be able to perform tasks perfectly, if at all, and seniors are likely to get frustrated is an activity is too difficult. It will take constant trial and error to create and modify activities to meet an elder's shifting capabilities.

The Community for Family Caregivers is an online forum created to Support Caregivers of Elderly and Aging Parents. The material of this web site is provided for informational purposes only. AgingCare.com does not provide medical advice, diagnosis or treatment; or legal, financial or any other professional services advice.

(Source: By Anne-Marie Botek, 14 December 2011, Agingcare.com)

New Research Focuses on Lowering Levels of Beta Amyloid

2011-12-29T10:09:00.006+08:00

Mounting evidence suggests that beta amyloid accumulation in the brain is an early biomarker and a critical event in the early progression of Alzheimer's. Researchers are targeting amyloid-based therapies to be given in earlier stages of the disease, perhaps even before symptoms emerge. While more research is needed, some scientists believe these therapies could reduce the risk of, and possibly prevent, cognitive impairment and dementia.

Researchers Look to Disease-Modifying Therapy to Ward Off, Possibly Prevent Alzheimer’s Disease

Just as statins help lower high cholesterol levels to reduce the risk of heart attacks, researchers are seeking a comparable approach for people with large amounts of beta amyloid, an abnormal protein in the brain commonly found in Alzheimer’s disease patients. Medicines would clear those proteins before any signs of memory loss or other early symptoms of Alzheimer’s appear.

Could amyloid-based drugs given at much earlier stages of Alzheimer’s-even before any clinical symptoms begin-reduce the risk and possibly prevent the emergence of cognitive impairment and dementia?

That is the central question of a provocative commentary in the Nov. 30 issue of Science Translational Medicine, written by a trio of researchers who cite how Alzheimer’s, which affects more than one out of every 10 individuals over the age of 65, is the only leading cause of death for which no disease modifying therapy exists.

Currently, most proposed Alzheimer’s drugs are tested in patients in the later stages of the disease, because no reliable medical test, brain imaging or other method currently exists to accurately detect the disease before initial symptoms appear. Recent clinical trial failures at the dementia stage have raised multiple questions about the current development of disease-modifying therapies, prompting a strategy to begin developing and testing drugs aimed at the initial stages of the disease rather than at the end stage of the illness.

Mounting evidence, the authors note, from natural history studies supports amyloid beta accumulation in the brain as an early biomarker and a critical event in the early progression of Alzheimer’s. Already, some studies have shown that a person’s brain may be damaged at least a decade prior to the first signs of Alzeimer’s symptoms. More than 50% of certain brain cells are already lost by the time a patient shows even the mildest cognitive impairment.

However, it remains unclear whether the buildup of amyloid beta protein (which accumulates in the areas of the brain responsible for learning and creating, retaining and extracting memories) is an early symptom or a cause of the disease. Several small monoclonal antibody studies that reduced the amyloid plaque burden have not shown any clear benefit in the limited number of patients treated at stages of mild to moderate dementia.

Titled “Testing the Right Target and Right Drug at the Right Stage,” the authors suggest specific amyloid-based therapies be directed at much earlier stages of Alzheimer’s-perhaps even before the emergence of clinical symptoms. “Furthermore, we argue that the field has sufficient tools to being secondary prevention trials—those conducted after the disease process has begun in hopes of preventing the emergence of symptoms—in asymptomatic individuals who are at risk for the progression of cognitive impairment and AD dementia.”

Still, one-third of the nation’s aging baby boomers show no signs of Alzheimer’s despite an amyloid burden, prompting the researchers to ask, “How do older individuals spend years with a ‘head full of amyloid’ and remain apparently healthy? Is amyloid ‘necessary but not sufficient’ to result in cognitive impairment?”

Clinical trials to test whether specific drugs can head off the disease at various stages of Alzheimer’s, and thinking about the disease in terms of primary, secondary and tertiary prevention, rather than lumping together all disease modifying treatments, is a first step.

The article’s lead author, Reisa Sperling, M.D., an Alzheimer’s specialist at Brigham and Women’s Hospital in Boston, said she hopes to launch a three-year study of an amyloid clearing medication in 1,000 patients age 70 or older who have no Alzheimer’s symptoms but have amyloid plaque in their brains. The clinical trial also would be a milestone as the first known anti-amyloid drug given to people without Alzheimer’s symptoms.

Dr. Sperling’s plan, which requires major government and industry funding, is among a trio of academic plans to pursue comparable research in populations not diagnosed with dementia, with a goal of launching studies next year, according to Maria Carrillo, M.D., senior director of medical and scientific relations for the Alzheimer’s Association.

"Although nothing is programmed or funded yet, we are having discussions with federal regulators, the National Institutes of Health and various experts, and I think in 2012 we may see the first clinical trials,” said Carrillo, adding that both the FDA and the EMA are involved in the discussions of pre-dementia clinical studies.

She also is optimistic that by next June the FDA could approve a brain imaging product for early amyloid plaque detection that possibly could rule out Alzheimer’s in those with no signs of the amyloid protein in their brain scans.

“The analogy with statins, where you are treating populations with no symptoms early on, is a good one,” said Carrillo, “because we can change the course of Alzheimer’s disease to where it can be delayed, detected early, understanding changes without cognitive impairment—even avoided altogether.”

(Source: By Ronald Rosenberg, 19 December 2011, Alzheimer’s Association)

Early Detection May Delay Alzheimer's Development Among Patients

2011-12-27T18:10:00.003+08:00

A Researcher has found A New Way To Approach Early Detection of Alzheimer's Disease.

The researcher at the University of the Basque Country (UPV/EHU) Xabier Elcoroaristizabal is looking for complementary genetic factors.

One of our genes is apolipoprotein E (APOE), which often appears with a variation which nobody would want to have: APOEe4, the main genetic risk factor for sporadic Alzheimer's disease (the most common form in which this disorder manifests itself and which is caused by a combination of hereditary and environmental factors).

It is estimated that at least 40 percent of the sporadic patients affected by this disease are carriers of APOEe4, but this also means that much more still remains to be studied.

Elcoroaristizabal has opened up a channel for making a start by analysing candidate genes, which always in combination with APOEe4, could help to explain more cases.

The long-term aim is to contribute towards the early detection of Alzheimer's disease by identifying signs that could be detectable in the very early phases. And, as Elcoroaristizabal explains, while there is no cure for this disorder, the alternative is to get ahead of it and delay its development.

"Certain preventive measures involving cognitive stimulation delay its appearance. There are even new drugs that could start to be used earlier. Today there is no solution, but the more we maintain a person's correct cognitive state, the better," he said.

The individuals who develop Alzheimer's go through a transition period first of all, and this could be the key moment for the effective application of preventive measures. This is mild cognitive impairment (MCI), in which slight cognitive alterations take place but do not affect everyday activities.

Among the different types of MCI, one affects memory almost exclusively (amnestic MCI), and those people who suffer from it have a high probability of developing the disorder. The difficult and interesting part is knowing which genetic components are linked to this impairment and also in determining by what percentage the risk of developing the disease increases, a task which Elcoroaristizabal has set himself.

"If we can identify which genes are involved and what susceptibility factors there are, preventive measures could be taken," he said.

So a contrast study has been carried out among a sample of patients with MCI, ones with Alzheimer's and healthy people. This can be used to observe the changes and narrow down the field for the zones to be studied, so that candidate genes can be sought there.

Elcoroaristizabal himself notes one example among the many others identified.

"It has been observed that the brain's capacity to control cholesterol levels seems to play a key role throughout the illness. So, protein encoding genes linked to this control have been analysed," he claimed.

In this quest for candidate genes, Elcoroaristizabal has confirmed that the APOEe4 genetic variation is, in fact, the main risk factor for developing Alzheimer's disease. But it does not end there; he has identified several genes which, as long as they are manifested in combination with APOEe4, could take us one step further towards the early detection of this disorder.

"Genes that in some way are connected with neurotransmission channels, oxidative stress or the effectiveness of oestrogens seem to be linked to a greater risk for APOEe4 carriers," he explains. Specifically, the candidate genes are as follows: COMT (neurotransmission), SOD2 (oxidative stress elimination) and ESR1 and ESR2 (oestrogen action facilitators).

His thesis is entitled 'Molecular markers in mild amnestic cognitive impairment and Alzheimer's disease' (Marcadores moleculares en deterioro cognitivo leve tipo amn sico y enfermedad de Alzheimer). An initial article on this can be read in the Journal BMC Neuroscience.

The study has been published in the Journal BMC Neuroscience (ANI).

(Source: ANI, 24 December 2011)

Alzheimer's Association® Successfully Advocates on Behalf of Constituents to Secure Funding for Alzheimer's Research and Programs

2011-12-27T17:18:00.003+08:00

Funding includes dollars for innovative Alzheimer's research and successful public private partnerships with the government to provide care and support to families

As the world's leading voluntary health organization advocating for Alzheimer's care, support and research, the Alzheimer's Association is pleased that Congress and President Obama have responded to calls by the Alzheimer's Association on behalf of people with Alzheimer's disease, caregivers, health professionals and researchers, to provide federal funding for several programs critical to the Alzheimer's community.

The Fiscal Year 2012 Omnibus Appropriations bill, that was passed last week and signed by President Obama today, includes funding for the National Alzheimer's Project Act (NAPA) Advisory Council on Alzheimer's Research, Care, and Services. NAPA mandates the development of the first-ever national plan to address the rapidly escalating Alzheimer's crisis and coordination of Alzheimer's disease efforts across the federal government. One year after enactment of NAPA, the Association is delighted that Congressional Appropriators supported the intent of Congress for robust implementation of the statute by providing $250,000 in funding for the Advisory Council. Leadership and foresight by Senate Labor, Health and Human Services, and Education Appropriations Subcommittee Chairman Tom Harkin (D-IA), Ranking Member Richard Shelby (R-AL), House Labor, Health and Human Services, and Education Appropriations Subcommittee Chairman Rep. Denny Rehberg (R-MT) and Ranking Member Rosa DeLauro (D-CT) is appreciated by the Alzheimer's Association and the millions impacted by this fatal disease.

"It is clear that the Alzheimer's Association's efforts on behalf of people living with Alzheimer's disease, families and health professionals, are being heard. We urgently need funding that will provide us with a greater understanding of Alzheimer's as well as provide care and support to those currently impacted," said Robert Egge, Vice President of Public Policy for the Alzheimer's Association. "Our hope is that the priority placed on Alzheimer's disease by the federal government will continue to increase to a level that is proportionate to the human and financial toll of this disease."

Continuing to set an example for successful programs, Congress intends to fund the National Alzheimer's Call Center, which is a helpline run by the Alzheimer's Association that is available 24-hours a day, 7 days a week to provide crisis counseling, care consultation, and information and referral services in 140 different languages for people with the disease, caregivers, families and professionals and all those impacted. Historically, federal funding for the National Alzheimer's Call Center has been included in the annual appropriations bill at $1 million. This productive private-public partnership has included a matching investment by the Alzheimer's Association to ensure effective support for people impacted by Alzheimer's disease. The Association is pleased that the program was included in the Administration on Aging (AoA) Aging Network Support Activities program for Fiscal Year 2012. While the specific funding level was not enumerated in the Omnibus bill, the intent of Congress is to continue this successful program.

Critical to changing the trajectory of Alzheimer's disease is research, and because of the Alzheimer's Association's advocacy efforts, an additional $12 million was directed to the Department of Defense (DoD) Peer-reviewed Alzheimer's Research Program. Established eight months ago with $15 million, the program focuses on innovative and outcome-oriented research that is relevant to military personnel and the Alzheimer's community. As a result, the well-designed and results-oriented program received strong support from House Defense Subcommittee Chairman C.W. Bill Young (R-FL) and Ranking Member Norm Dicks (D-WA), Congressman Jim Moran (D-VA) and Congressman Steve Israel (D-NY) helping to drive the added investment to continue this important program for Fiscal Year 2012. Their thoughtful leadership is valued by the Alzheimer's Association and our constituents.

In addition, on the research front, extensive advocacy by the Alzheimer's Association was successful in ensuring that biomedical research remains a priority. The National Institutes of Health (NIH) saw an additional $299 million added to their budget, bringing the total to $30.6 billion. The bill also established for the first time the new National Center for Advancing Translational Sciences (NCATS). As part of the funding directed to the NIH through the Omnibus spending bill, $10 million was designated for a new program within NCATS – the Cures Acceleration Network (CAN). NCATS and CAN will provide vital new approaches to moving high need medical cures through the drug development pipeline faster. Given the estimated 5.4 million Americans living with Alzheimer's disease and 16 million people projected to have the disease by mid-century, according to the Alzheimer's Association's 2011 Alzheimer's Disease Facts and Figures report, these innovative processes are an important opportunity for Alzheimer's biomarker and early detection research. The funding commitment to the NIH, along with the Agriculture Appropriations bill passage in November, that provided the Food and Drug Administration (FDA) funding at $2.5 billion (a $50 million increase over FY11), will support critical FDA responsibilities, including the review of potential breakthrough therapies and diagnostics for those with Alzheimer's disease.

"Hope of changing the trajectory of Alzheimer's lies in the discovery of effective treatments and identifying Alzheimer's at an early pathology point," said William Thies, chief medical and scientific officer of the Alzheimer's Association. "NIH, FDA and DoD funding for Alzheimer's must increase as a national priority so that we can advance medical progress, improve the lives of people with Alzheimer's and reduce cost incurred by the federal government in the future."

Funded at the same level as the previous year, the Healthy Brain Initiative at the Centers for Disease Control and prevention (CDC) is another example of successful public-private partnership between the Alzheimer's Association and the federal government. Created by Congress in fiscal year 2005, the partnership between the CDC and the Alzheimer's Association educates both the public and health professionals about ways to reduce the risk of developing Alzheimer's by maintaining a healthy lifestyle.

The Alzheimer's community also saw a significant decrease in State grants to support community programs for the coming year, with only $4.018 million being designated for the Alzheimer's Disease Demonstration Program at the AoA. The Alzheimer's Association is disappointed to see a 65 percent cut to a program that helps develop innovative and evidence based approaches to helping people with the disease and their families.

Alzheimer's Association
The Alzheimer's Association is the world's leading voluntary health organization in Alzheimer's care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's. For more information, visit www.alz.org.

(Source: Washington, 23 December 2011 - PRNewswire-USNewswire.)

Thinner Brains Could Signal Alzheimer's, Study Suggests

2011-12-23T11:17:00.003+08:00

New research suggests that the outer edges of the brain are thinner in older people who may be destined to develop Alzheimer's disease, but there's currently no way to use the information to help people fend off dementia.

Still, the findings could help researchers test Alzheimer's medications by allowing them to track the progression of the disease, said study co-author Dr. Brad Dickerson, an associate professor of neurology at Harvard Medical School.

Alzheimer's disease is the sixth leading cause of death in the United States, according to the Alzheimer's Association, and the number of deaths has risen in recent years. There's no cure for the disease.

In the new study, researchers focused on the thickness of the edges of the brain, known as the cortex. "We're looking at the parts of the cortex that are particularly vulnerable to Alzheimer's disease, parts that are important for memory, problem-solving skills and higher-language functions," Dickerson said.

Previous research found that several areas of the cortex were smaller in people with dementia from Alzheimer's. "It's like an orange that's shriveling. The thickness of the outer skin might get thinner as it dries out," Dickerson said.

In the new study, researchers examined the MRI brain scans of 159 people with an average age of 76; about half were men. Three years later, the participants took tests designed to measure how their brains were functioning.

The findings appear in the 21 December 2011 online issue of the Journal Neurology.

The 15 percent of participants with the thinnest brain areas performed the worst on the tests: About one in five of them experienced cognitive decline. They also showed increases in signs of abnormal spinal fluid, a possible sign of developing Alzheimer's disease.

"That suggests they may be developing symptoms," Dickerson said.

A lower number - 7 percent - of the participants in the middle range of brain thinness experienced cognitive decline. None of the people with the least thin brain areas developed problems.

So are the scans appropriate as tools to figure out whether patients are on the road to Alzheimer's?

Cost doesn't appear to be a major challenge at this point. It's not clear how much the MRI scans might cost at doctor's offices, Dickerson said. However, they're only a few hundred dollars each in the research world.

Also, many older people already receive MRI scans of the brain for other reasons, said Dr. Raj Shah, medical director of the Rush Memory Clinic, in Chicago.

But with no cure for Alzheimer's, the best use for the scans will be to help researchers figure out if medications work, Dickerson said.

Cathy Roe, an Assistant Professor of Neurology at the Knight Alzheimer's Disease Research Center at Washington University School of Medicine, in St. Louis, said the findings could have value down the line. "Right now, there is not much we can do to delay the progression of dementia," said Roe, who's familiar with the findings. "But once effective treatments are identified, this research could help to identify which patients should receive that treatment and when they should receive it."

(Source: HealthDayNews, 21 December 2011)

ADI Newsletter "Global Perspective" December 2011 Issue, Vol. 21 No. 4

2011-12-14T16:34:00.004+08:00

Dear Caregivers/Members,

The December 2011 Newsletter "Global Perspective" from the Alzheimer's Disease International (ADI) is now available online, click at:
Global Perspective, December 2011 Vol. 21 No. 4

This issue includes:
* World Alzheimer's Day 2011
* Launch of the World Alzheimer Report 2011
* Antipsychotic drug treatment for dementia symptoms

As Christmas is around the corner, "WISHING ALL OF YOU A VERY HAPPY CHRISTMAS AND NEW YEAR".

Alzheimer's Australia, Bupa Health Launch Brain Health App in the UK

2011-12-12T06:54:00.003+08:00

The Bupa Health Foundation and Alzheimer's Australia have announced the UK launch of a world-first brain health app, the latest digital tool to help in the fight against dementia.

Based on latest research that links brain health and a reduced risk of dementia, to a healthy heart and cardiovascular system, 'BrainyApp' is the first dementia risk reduction iPhone app designed to help people monitor and improve their brain-heart health.

The new app, which was designed by Alzheimer's Australia and Bupa Health Foundation, has already knocked Facebook off the number one spot in the Australia and New Zealand Top Free Apps list and has clocked up more than 130,000 downloads down under.

Now available to people in the UK, 'BrainyApp' helps users monitor and improve the physical, mental, dietary and social aspects of their lifestyle.

There are currently 750,000 people living with dementia in the UK and this is predicted to rise to over a million by 2021. Delaying the onset of dementia by just five years would reduce deaths directly attributable to dementia by 30,000 a year.

Jeremy Hughes, Chief Executive, Alzheimer's Society, said: "Most people know how to reduce their risk of heart disease, diabetes and stroke but they don't realise that the same healthy lifestyle choices may also lower the risk of developing Alzheimer's disease and other kinds of dementia. The idea is that what is good for the heart is also good for the brain."

'BrainyApp' allows users to take a brain-heart health survey about their diet, exercise patterns and lifestyle. It then provides suggestions and ideas about how to make improvements to each. It also includes all-new brain games, and encourages users to build brain-heart points by staying physically and mentally active, socialising with friends and family, and sharing their progress on Facebook.

One of the brain games - 'Word Tennis' - requires players to unscramble anagrams in order to move a paddle and hit a ball back to their opponent.

Director of Dementia Care for Bupa Care Services, Dr Graham Stokes, said: "There is evidence to show that keeping the mind exercised can stave off the onset of dementia but 'BrainyApp' highlights that good physical health also has a part to play. Best of all it's good fun."

'BrainyApp' is available as a free download for users of iPhone, iPod and iPad devices from the App Store. There are plans to develop an Android version in early 2012.

Download

App Features:

1. Brain health survey – see what your brain health score is and receive personalised recommendations on what you can do to improve your brain health.
2. Brain games – give your brain a work out with interesting and challenging games.
3. Activities – add to your brain health points with a range of activities including exercise, eating well, getting health checks, keeping your mind active and managing your smoking and alcohol intake.
4. Monitor your Brain Health Points and track your progress over time.
5. Get a daily fact sent to you from BrainyApp.
6. Share facts and your brain health scores with friends and family.

Watch Video : Alzheimer's Australia-2011 BrainyApp Info

(Source: Bupa Health Foundation, Published on December 6, 2011)

The Latest Brain Discoveries From Alzheimer's to Autism to Stroke

2011-12-09T15:07:00.001+08:00

The brains of the mice that Bradley Hyman keeps in his sprawling lab at an old naval base in Boston offer a window, literally and figuratively, into the mysterious damage that causes Alzheimer's disease. When each mouse reaches a few months of age, one of the lab workers carefully creates an opening in its skull and places a tiny glass window over the hole. Day after day, week after week, a powerful microscope is trained on the brain, searching for ugly clumps of sticky protein fragments like those that litter the brains of elderly people who have died of Alzheimer's. "It's like time-lapse photography," says Hyman, director of the Massachusetts Alzheimer's Disease Research Center at Harvard Medical School. When the ugly plaques appear—and they always do, as the mice carry genes engineered to produce them—nearby brain cells begin to wither and die, interrupting the flow of information. Next, waves of cells die off.

Hyman's microscope is one of several new technologies that promise to revolutionize the struggle to understand and beat Alzheimer's, which now afflicts more than 5 million Americans. Worldwide, a staggering 1 percent of all economic output is spent caring for and treating people with it and other types of dementia, according to Alzheimer's Disease International, the umbrella group of Alzheimer's associations around the globe. Meanwhile, just four drugs have been approved by the Food and Drug Administration to battle the disease, and all address symptoms only, not the poorly understood causes. Over the past decade, billions of dollars have been poured into researching drug after initially-promising drug, and nearly all have been disappointing in large clinical trials.

"When you can watch the brain over time, we see now, we didn't have the details right," says Hyman, who holds out great hope that his microscope studies will help correct that. One assumption has been that the plaques themselves, accretions of a protein fragment called beta amyloid, harm the brain. Instead, it appears that the individual sticky strands that eventually form the plaques damage neurons, and that the plaques are a sign of a brain long under siege.

For years, researchers have debated whether the brains of people who develop Alzheimer's produce excess beta amyloid or they're simply bad at clearing it. In December, researchers at Washington University School of Medicine in St. Louis provided strong evidence for the latter theory. They measured radioactively labeled beta amyloid visible in the spinal fluid of healthy older adults and people with Alzheimer's. Both groups appeared to produce the same amount, but the ill individuals cleared the substance from their brains into their spinal fluid at a rate about 30 percent slower. Moreover, since autopsy studies find that some people with no cognitive symptoms of Alzheimer's carry a substantial plaque load, the body may possess a varying capacity to withstand beta amyloid's assault.

Following on the success of periodic cholesterol testing, which has revolutionized heart care, researchers are experimenting with measuring beta amyloid via brain scans, spinal taps, and blood tests. Early results offer hope that, someday, physicians will be able to screen the middle-aged for the hallmarks of pre-Alzheimer's. "It's critical to identify people at risk," says Reisa Sperling, who is using brain PET scans of beta amyloid at Brigham and Women's Hospital in Boston to study the impact in people who are not showing symptoms. She's concerned that right now drug treatment starts five or 10 years too late. An FDA advisory committee recommended in January that the agency approve a PET scan that could be helpful in diagnosing people who already have the plaques.

Of course, without effective drugs, early detection offers little solace. Most of the recently failed drugs aimed to interrupt production of beta amyloid by blocking the enzyme that produces it. However, researchers have opened a new front in the battle, targeting the synapses between neurons, which new research shows may be the first structures to deteriorate. Another approach, based on the theory that the body must have natural defenses if most people don't get Alzheimer's, seeks to train the immune system to attack beta amyloid. But all of the new drugs have been given to patients who already show cognitive symptoms. Adrian Ivinson, director of the Harvard NeuroDiscovery Center, which focuses on degenerative brain diseases, thinks some of the failed drugs should be retested in asymptomatic individuals who show beta amyloid on brain scans or in spinal fluid tests. "The implication of all this work is we have to get [the drugs] into people before they're patients," he says. "They have a silent disease."

What about prevention? There is accumulating evidence that exercise, eating fish or other sources of omega-3 fatty acids, and remaining intellectually and socially engaged throughout life reduce the risk of Alzheimer's. But last year a panel assembled by the National Institutes of Health concluded that the evidence on lifestyle interventions is inconsistent and inconclusive, pretty much across the board. "There are suggestions that some things might be effective, but there isn't strong, high-grade evidence for any of them," says Neil Buckholtz, chief of the dementias of aging branch of the National Institute on Aging. The NIA is now running several large studies to see if exercise, diet, or social or intellectual engagement will reduce risk.

Having had a stroke substantially raises the odds of Alzheimer's, as does having diabetes. But the biggest known risk factor is one people can do nothing about: a family history of the disease. People carrying one copy of variations in a gene called APOE are at about a threefold risk, while those carrying two copies have a whopping 12-fold risk. But it appears possible now that many genes, perhaps even a hundred, may each confer a tiny increased risk of developing Alzheimer's. Still, Rudy Tanzi, an Alzheimer's geneticist at Harvard Medical School, is hopeful that by 2020, a screen of a person's genome will reliably estimate his or her risk of developing the disease. Ideally, the people at highest risk will then have scans or spinal fluid or blood tests regularly to detect accumulating beta amyloid. Once it is seen, they'll begin taking the equivalent of a "statin for the brain" to reduce the load. And Alzheimer's will become as preventable as heart disease is today.

(Source: US News & World Report, By Brian Vastag, Kathryn Roethel, Angela Haupt, Donna Banks, Keith Sinzinger, December 7, 2011)

Breakthrough Closer for Alzheimer's Treatment After Vaccine Success

2011-12-09T14:54:00.004+08:00

AUSTRALIAN researchers have proved that an Alzheimer's vaccine could halt the disease – and even see the return of some losses – well after the symptoms first appear.

Lars Ittner from the Alzheimer's and Parkinson's disease laboratory at Sydney University said it was the first time researchers had proved a vaccine targeting the tau protein in mice could be effective after the disease had set in.

Tau proteins stabilise microtubules, which help maintain cell structure. When defective, they can result in dementias such as Alzheimer's disease.

Professor Ittner said targeting the tau protein in younger animals before the onset of the disease was a different approach, as most researchers worked with animals after the onset of Alzheimer's.

"What we tried to do was to work with older mice with a lot of damage," he said. "Because in people, by the time they realise their symptoms are Alzheimer's, a lot of the damage has already been done."

In a paper in the scientific journal PLoS ONE today, the research team says the novel approach worked, producing some of the most improved results recorded in mice with advanced dementia.

"The older group with the very advanced Alzheimer's actually benefited the most," Professor Ittner said.

While human trials are at least five years away, he said such positive results from the animal trials were a surprise.

Three groups of mice were used in the study. Each group was formed according to age – six months, 12 months and 18 months. The older the group, the more advanced the the stage of Alzheimer's disease.

The mice were treated for 10 months and assessed at the end of that period. Professor Ittner said there were also signs the animals had regained some losses such as weight loss and activity levels.

"But this was limited as, when there's damage to a neuron, it's gone. It doesn't regenerate," he said.

The team, which is already collaborating with the US pharmaceutical industry in the quest to develop a vaccine, aims to create a monthly injection which would become part of a broader treatment of the disease.

According to Alzheimer's Australia about 269,000 Australians live with dementia. Without a significant medical breakthrough, it is forecast about 981,000 Australians will be living with dementia by 2050.

Dementia is used to describe a large group of illnesses which cause a progressive decline, including a loss of memory, intellect, rationality, social skills and physical functioning. Alzheimer's disease is the most common form of dementia, accounting for up to 70 per cent of cases.

Also read -> Alzheimer's vaccine cures memory of mice

(Source: Bridie Smith, Sydney Morning Herald, December 9, 2011)

Latest Study : Risk for Dementia Rises When Diabetes, Depression Meet

2011-12-07T06:08:00.002+08:00

When people with type 2 diabetes also struggle with depression, their odds for a third worrisome condition - dementia- goes up markedly, a new study suggests.

Specifically, patients with type 2 diabetes are twice as likely to develop dementia three to five years after being diagnosed with depression compared to nondepressed people with diabetes, researchers found.

"We've known for years that diabetes is a risk factor for dementia," explained study lead author Dr. Wayne Katon, a professor and vice chair of the department of psychiatry and behavioral sciences at the University of Washington's School of Public Health in Seattle. "In fact, having diabetes itself probably doubles the risk for dementia," Katon added.

"We've also known that a very common accompanying condition with diabetes is depression," Katon said. "Some 20 percent of diabetics have depression. And now our data suggests that if you do have depression in addition to diabetes, it actually doubles again the already increased risk for dementia that diabetic patients face."

However, the study authors noted that the absolute risk of dementia for any one person with depression and diabetes remains relatively small - about one in 50.

Katon and his colleagues published their research, which was supported by the U.S. National Institutes of Health-funded Diabetes & Aging Study and the Diabetes Study of Northern California, in the Dec. 5 online edition of Archives of General Psychiatry.

The authors noted that depression and diabetes are among the most prevalent health issues facing American seniors.

What's more, each of the two conditions seem to independently raise the risk for developing the other: Being diabetic bumps up the likelihood of becoming depressed, while being depressed boosts the risk for developing diabetes.

In the new study, the researchers focused on more than 19,000 California residents with diabetes between the ages of 30 and 75.

Nearly one in five of the patients were also deemed to be experiencing "clinically significant" depression, the authors noted.

After monitoring for the onset of dementia over a three- to five-year period, the research team found that just over 2 percent of those who had both diabetes and depression went on to develop one or more forms of dementia, including Alzheimer's disease.

By contrast, just 1 percent of patients who had diabetes alone ended up developing dementia during that period.

But the authors also noted that many of the things that can boost the odds for depression among diabetic patients, such as eating a poor diet, maintaining a sedentary lifestyle and/or smoking, are modifiable behaviors. This means that patients and physicians alike have some clear targets for interventions to lower depression risk, and possibly dementia risk as well.

"So the important thing to focus on here is that there are very effective treatments for depression," said Katon. "And so if you're a diabetic who does have depression it's very important to get it attended to. Just as important as getting your diabetes itself treated."

Dr. Robert Friedland, chair of neurology at the University of Louisville School of Medicine in Louisville, Ky., agreed.

"It is not surprising that they should find a relationship between depression in diabetics and a higher risk for dementia," he said. "But I would point out that although both diabetes and dementia have genetic influences, there are also clear things people can do to lower their risk for both. For example, avoiding obesity by eating a relatively low-fat diet and engaging in regular physical exercise can help to prevent both diabetes and depression. And, therefore, dementia as well."

There's more on the diabetes-depression link at the American Diabetes Association.

(Source: HealthDay News, 5 December 2011)

How to Respond to Wandering Attempts in Alzheimer's

2011-12-06T05:59:00.005+08:00

What should you say or do if someone with Alzheimer's or another dementia is trying to wander away? For example, imagine that your father with dementia, who is living with you in your home, starts to pace around and try to go outside. Here are some practical approaches you may utilize in response.

5 Strategies to Employ:

1. Ask Him Questions In A Non-Threatening Manner
Ask him how you can help and where he's going. Perhaps he's just a bit restless and unsettled. Maybe he'll respond with an answer that will give you insight into what he's looking for or where he wants to go.

2. Don't Argue
It's almost universally not helpful to argue with someone with dementia who is intent on doing something. Arguing will likely increase his agitation because in his reality, what you're saying doesn't make any sense. Rather, just talk with him and validate3 his feelings. For example, if he is talking about needing to go to work, ask him about his job. You can ask him what he liked the most about his job, or talk about the benefits of retirement.

3. Remember Your Non-Verbals
If you're standing there with your hands on your hips and a frustrated look on your face, you'll have less success in persuading your loved one to do anything. The words that you speak may or may not make sense to him, but your body language will send clear messages to him. Speak in a calm tone of voice and smile. Be gentle, and if physical touch is something your dad is used to, a little pat on the shoulder or holding of his hand may reassure h

4. Distract
Distraction is often very effective. You can ask him to eat a bite of dinner before he leaves, for example. You could also let him know that he may need to return to his room to grab his sweater or jacket before he leaves. Perhaps there's a football game on tv you can flip on when he returns with his sweater. Or, you can remind him that his friend Joe may be stopping by to chat with him so he may want to stay home for his visit.

5. Walk With Him
If it's a nice day, take a break from what you're doing and go with him. I realize that the timing may not always be ideal, but perhaps he simply needs to go for a walk. Take your cell phone with you before you leave in case he's unwilling to come back home with you or is too tired to walk any further.

What if it's cold or raining out and your father still is agitated and determined to go outside?
Grab a jacket for both of you, go outside and walk with him. I've seen many people with Alzheimer's walk for a brief time outside, turn to their loved one who came out with them and say, "Let's go inside. It's cold out here!" Again, take your cell phone or notify someone that you're going for a walk with him.

(Sources: By Esther Heerema, About.com Guide, Updated December 01, 2011)

How To Control Alzheimer's Wandering

2011-12-05T19:42:00.006+08:00

Alzheimer's disease causes sufferers to become disoriented, confused and afraid. The disease can erase memories of once-familiar surroundings, and as a result, Alzheimer's patients often wander away from home. In fact, the Alzheimer's Association estimates that 60% of Alzheimer's patients wander away from home. The stress can weigh heavily on caregivers and family.

It is not possible to completely prevent wandering in people with Alzheimer's and dementia, but caregivers can minimize the risk.

Here are some techniques to try:

1. Install Wandering-Prevention Locks
Install locks and escape prevention devices on doors, windows and gate. These products require complex maneuvers to open doors, thus making it difficult for Alzheimer's and dementia patients to leave. For example, if your loved one tends to unlock doors, install sliding bolt locks out of your loved one's line of sight.

2. Install Alarms
There are many wandering prevention alarms on the market that can alert you that your loved one is trying to get out. These devices include motion detectors, pressure-sensitive alarm mats at the door, and warning bells on doors.

3. Disguise Escape Routes
Camouflaging doors and windows inhibits the Alzheimer patient's ability to find a way out. Paint doors the same color as walls, or hang curtains on windows that match the color of walls, so they blend in with surroundings, and make them less visible.

4. Provide A Safe Place To Wander
Provide a safe place in your home or yard for walking or exploration — such as a path through the rooms of your house or a circular trail through a fenced backyard.

5. Use Visual Cues
People who have Alzheimer's often forget where they are, even inside their own homes. Visual reminders provide clues and trigger memories. For example, post descriptive photos on the doors to various rooms, such as the bathroom, and kitchen. Even Stop signs at doors have been reported to help.

6. Look for Triggers and Plan Distractions
Many people with Alzheimer's disease have a pattern to their behaviors. Watch for triggers, such as a certain time of day. (Many people with Alzheimer's become agitated or fear just before or after sundown, known as Sundowner's syndrome) If your loved one tends to wander at the same time every day, a planned activity at that hour could stem the wandering.

7. Hide keys
In addition to wandering on foot, people with Alzheimer's might attempt to drive. Store and hide keys to cars and doors. Also, keep coats and shoes out of sight.

8. Warn Neighbors and Authorities
Caregivers often don't know their loved ones are missing before someone finds them. If neighbors are made aware of the situation, they can be on the look-out. Notify neighbors and police and make sure they have your contact information.

9. Use A Tracking Device
If your loved one wanders, a GPS or radio frequency device can help emergency personnel, find him or her quickly. The Alzheimer's patient wears a bracelet or ankle tracking device - a personal transmitter that tracks the person's location. Many communities have a program called Project Lifesaver, (link to Project Lifesaver article) to track and locate wanderers. Check with your police station to find out if a program is available in your area.

10. ID Bracelets
The Alzheimer's Association operates a nationwide identification system called Safe Return . The person with Alzheimer's wears an engraved ID bracelet or necklace with a phone number to call if they're found. Their name is entered into a national database, where anyone can call 24 hours a day.

11. Prepare for A Search
Keep a recent photo and detailed physical description of the person readily available. Also have medical and health information, and vehicle information on hand.

(Source: By Marlo Sollitto, Agingcare.com)

How-To Take the Stress Out of Getting Dressed with Dementia

2011-12-05T19:13:00.004+08:00

Alzheimer's can turn even the simplest of tasks into great trials. In the middle and later stages of the disease, many people have difficulty dressing themselves.

Here are a few pointers to help simplify the task of helping a person with Alzheimer's get dressed.

1. Shop Together
If at all possible you should take the person with Alzheimer's disease when you shop for their clothes. Letting them select some of their favorite items will make the new clothes seem familiar and they will be more likely to wear them.

2. Buy Duplicates
If your parent often insists on wearing that "favorite outfit" constantly, consider buying several identical sets.

3. Look for Simplicity
Choose clothing that is easy to get on and off. Elastic waists and Velcro enclosures minimize struggles with buttons and zippers.

4. Give Them Choices
This can be tricky because a person with dementia can have trouble making decisions if there are too many options present. To avoid frustration and potential tantrums, give them a few choices, preferably no more than three. Lay out the clothes on a bed or dresser so the person with Alzheimer's can easily see them.

5. Give Them Time
Depending on how advanced the person's dementia is, it may take longer than normal for them to select their outfit and dress themselves. Be patient, and schedule enough time so that delays in the dressing process don't interfere with other plans.

6. Establish Order
Arrange the clothes in the order they are to be put on to help the person move through the process.

7. Be Positive and Open
Encouragement and compliments go a long way to helping a person with Alzheimer's disease feel content with their clothing choices. This includes supporting decisions that you may not necessarily agree with. As long as it doesn't endanger the elderly person, let them wear a dress to bed or a sweatshirt in warm weather.

(Source: By Anne-Marie Botek, 16 November 2011, Agingcare.com)

As Alzheimer's Advances, Couple Finds Acceptance

2011-12-01T11:56:00.029+08:00

Former Pilot Alan Romatowski Faces Increased Obstacles

When diagnosed with Alzheimer's disease at age 56, airline pilot Alan Romatowski was determined to remain productive, even if people could no longer depend on him to shepherd them across the country in Boeing 737s.

The Middlesex, Butler County, resident threw himself into volunteer work like he'd never done before. He made speaking appearances for the Alzheimer's Association in front of hundreds of people. He took whatever part-time work he could to help replace his US Airways income for his wife and children.

But as Alan passes through his fifth holiday season since being grounded by the devastating disease in the prime of his career, the productive work and most of the volunteering is gone. Stripped of his driver's license, he's alone much of the time in a home surrounded by woods, watching CNN for hours while playing with cats.

The good news is his memory is intact and he can often carry on a conversation well. Alzheimer's has eroded the 60-year-old's functioning more slowly than is the case for many patients -- he knows who everyone is, recalls what happened yesterday, is aware of his condition.

But that lucidity increasingly competes with fog. Alan strives to be the jovial joke-teller he's always been, but he stammers more than ever, forgetting obvious words. Simple tasks such as washing dishes and bagging groceries can confuse him. He becomes restless, and wife Josie finds it harder all the time to keep him contentedly occupied.

But if in some ways 2011 has been the toughest year for the Romatowskis since Alzheimer's settled into their spacious, suburban household, it has also brought a more mature understanding of how to live with the affliction.

After spending a year angrily denying that dementia symptoms had robbed him of his ability to drive his pickup truck safely or ride his beloved motorcycle, Alan now acknowledges that giving up his keys -- an action forced by his doctors -- was probably best for everyone.

Most all family responsibilities, from earning income from her Route 8 gift shop to doing chores, have fallen to Josie, his wife of 23 years. That's in addition to the burden of serving as a caregiver.

Not long ago, that all felt like too much to her. The onetime flight attendant, who fell in the 1980s for the Alan she knew as a smooth, confident pilot, would sometimes leave the house just so she could cry alone in her car in frustration. But after so many days of struggling through, then seeing she could make it to day's end and do it again and still keep her family, business and sanity intact, she realized she didn't have to feel defeated.

"I guess the big word is acceptance," she said in describing a recent awakening to how to live with a spouse's Alzheimer's. "I find I can get through the day without becoming overly emotional or overly frustrated. ... You find pleasures where you can."

Alan is not the normal Alzheimer's patient. An estimated 5.4 million Americans have the disease, but only a few hundred thousand are under age 65 and have his "younger-onset" version. The most prominent of those, highly successful University of Tennessee women's basketball coach Pat Summitt, received her diagnosis this year and is a year younger than Alan.

From the time his illness was confirmed at the University of Pittsburgh's Alzheimer Disease Research Center in September 2007, Alan became committed to raising Alzheimer's awareness. For the Alzheimer's Association, he served on a national advisory committee made up of people in early stages of the disease.

He also sought to enlighten the public about the disease by sharing his progress and struggle with it through the Pittsburgh Post-Gazette since 2008. It's become a less comfortable story for him.

Sitting next to his wife on a sofa in Glade Run United Presbyterian Church, the hub of a Meals on Wheels program in which he still volunteers once a week, Alan's arms were folded or fingertips tapping together as he described more recent experiences.

"I can still hold a conversation, but I get these senior moments more and more where the words don't come out," he said quietly while looking down.

His words flowed fine at that moment, but he also confessed it's become hard to read and retain anything. A task like raking leaves around their 5-acre property overwhelms him. He sees himself as a burden to his wife and stepdaughter, who lives with them, because he relies on them to drive him everywhere.

"I say I'm resigned to it, but that doesn't mean it's easy," he says, referring to his loss of driving, but it's just as applicable to the rest of what he's given up.

Earlier this year, he was both volunteering and doing part-time paid kitchen work at St. John Specialty Care Center, a nursing home in Mars. Those positions have ended, as has part-time work he enjoyed for nearly two years interacting with customers by providing food samples at the Costco in Cranberry.

When Alan started working at Costco, using his gift of gab and easy smile, it was hard for others to notice he had dementia, said his supervisor, Maria Jarvis of Club Demonstration Services. Once co-workers were aware of the disease, they helped look out for him. In recent months, they could no longer cover for his fogginess.

"One day he would seem 'with it,' like he was focused, and then another he would come in and it almost seemed like he was lost, like he didn't know where he was," Ms. Jarvis explained. She told Josie recently that giving Alan hours to work was no longer feasible, although Ms. Jarvis didn't want to tell him that directly.

While he can't drive for Meals on Wheels, Josie drops him off at the church every Wednesday morning to handle food deliveries. He rides alongside a driver in his 90s. Even there, he's not as sharp as he used to be, occasionally needing reminders from the older man of what to do with the meals, but the staff admire him and aim to help him remain a contributor as long as possible.

The Alzheimer's Association estimates there are some 15 million unpaid caregivers like Josie Romatowski for people with dementia. It is said that the disease is harder on them than on those it afflicts, especially as patients lose track of what's going on.

Among other difficulties in the past year, Josie has watched her husband get lost in supermarkets; curse at the microwave when it didn't do what he wanted; and shred documents she needed when Alan mixed them up with worthless papers she gave him to destroy to keep him busy. He's tried to repair things around the house, as he once did, only to make them worse. When confused or frustrated, he has lashed out, swearing and blaming others.

To relieve the frustration, Josie sometimes swaps stories about such incidents with other members of a local Alzheimer's Association support group, all of them wives who can relate. She even feels fortunate after such discussions, when hearing from others that their husbands can no longer carry on a conversation.

For four-plus years, she's watched how hard her husband has battled the disease, feeling admiration at his persistence while at the same time becoming more exasperated by Alan's behavior -- as though she had an adult-size 4-year-old child.

"He's kind of at an odd point," she said several months ago. "He really can't do too much, but he's not at the point yet where that doesn't bother him."

As a commercial airline pilot, Alan had to function mentally at such a high level for nearly three decades that his doctors believe it's given him more protection from the disease than is often the case. Alzheimer's affects everyone differently, in both pace and symptoms, and he's staved off the worst symptoms better than many.

"It's been a remarkably slow progression up to now, but this year is a little bit of a turning point for him," said Lori Macedonia, clinical coordinator of Pitt's Alzheimer Disease Research Center, where Alan receives an annual evaluation.

While Josie is increasingly worried about maintaining her gift store as Alan declines, Ms. Macedonia said a caregiver's ability to have her own outlet away from the disease has importance of its own. That sense of occasional freedom and use of a support group with whom to share struggles can be the biggest assets for someone like Josie.

"It's nice to know we're all in it together," Josie agrees.

When Alan was called upon as more of a public spokesman for Alzheimer's, the disease would more often make its way into conversations at home. It's most likely to come up now when the Romatowskis drive to the ADRC in Oakland, where in addition to evaluations, Alan receives a transfusion every 13 weeks of an experimental drug.

He reclines while Bapineuzumab is pumped into his system as part of an international study of its effectiveness. Preliminary results on use of the drug showed it could reduce the amyloid plaque in the brain that has been linked to Alzheimer's, though there's yet to be evidence that doing so restores individuals' mental abilities.

Alan had an earlier role in the study in which he received either the drug or a placebo, and he still doesn't know which. He and Josie are glad to know he's getting the real thing now, though they have no illusion of miracles.

"It's not something that's going to be an overnight fix," he says, sounding cautious like an academic researcher. "I'm not looking around the corner to see if there's going to be a major change in my cognition."

He also takes a couple of daily pills, Razadyne and Namenda, that can slow symptoms, though there's no guarantee.

Josie is agnostic about all these efforts, though there's nothing to do but try.

"People ask me 'Do the medicines work?' and I really don't know how to respond," she explains. "I don't know if he wasn't taking the medicine, if it would be worse. I don't know if the infusion is staving off progression. ... I do know he's declining."

But unlike before, she believes it's a decline she can live with. The couple still enjoy going out for meals. They were able to spend a summer week relaxing alone at their Edinboro Lake cottage, forgetting troubles. Old friends of Alan's occasionally visit him at home, though some have stopped, apparently because they're uncomfortable around him.

The disease has also robbed Alan of the relationship he wishes he had with his son, Yuri, a college freshman. In addition, he regrets that there's little he can do now to assist the family's income.

Josie worries about finances too, but also feels a sense of relief from that once all-consuming weight of Alzheimer's. She remembers feeling swallowed "in a black hole" by the fear of the future. But it is often preached that the key to battling the disease is dealing with it day to day.

She's succeeded in that, finally, by the repetition of assisting her husband and doing what she needs for herself without drowning.

"Now the days have piled up behind us, while two years ago there were days where I didn't think I could get through that day," she says. "Before, you didn't know if there was life after Alzheimer's, but there is ... for both of us."

(Source: alzheimers_enews@alz.org -By Gary Rotstein, Pittsburgh Post-Gazette, Sunday, November 27, 2011.)

Medications and Patients with Alzheimer’s Disease – What to Avoid

2011-11-23T05:58:00.007+08:00

Doctors are often asked whether there are any medications that someone with Alzheimer’s disease should avoid. Patients with Alzheimer’s disease may need medicines to treat symptoms of the disease, as well as for other health problems such as bladder incontinence, mood disturbances, high blood pressure, etc… However, when a person takes many medications, there is an increased risk of adverse effects, including confusion, mood swings, sleepiness, and worsening memory problems. Some medications can worsen symptoms of Alzheimer’s disease and should be avoided, if at all possible.

Sedatives and Sleep Aids:
Some sedatives or hypnotics, such as benzodiazepines and barbiturates, can cause drowsiness, confusion, increased cognitive impairment, slowed reaction, and worsening balance leading to falls. Sleep aids usually have the same effects. Examples of sedatives to avoid include the benzodiazepines diazepam (Valium), lorazepam (Aivan), temazepam(Restoril), triazolam (Halcion), and sleep aids zolpidem (Ambien), eszopiclone (Lunesta), and zaleplon (Sonata).

Antidepressants:

Certain antidepressants, such as the older tricyclic antidepressants amitriptyline (Elavil), nortriptyline (Pamelor), andimipramine (Tofranil), can cause sedation and worsening cognition. The tricyclic antidepressants have anticholinergic effects, meaning that they can further suppress the activity of acetylcholine, one of the main brain cell messenger chemicals whose activity is reduced by Alzheimer’s disease. For low mood and irritability in patients with Alzheimer’s, the SSRI (selective serotonin reuptake inhibitor) antidepressants including citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft) and the SARI (serotonin antagonist reuptake inhibitor) such as trazodone (Desyrel) can be considered instead.

Antipsychotics:

Antipychotics are sometimes given to treat behavioral symptoms such as agitation, aggressiveness, hallucinations and delusions. However, both the older antipsychotic drugs such as haloperidol (Haldol) and the newer atypical antipsychotics such as resperidone (Risperdal), olanzepine (Zyprexa) can cause serious side effects including sedation, confusion, and sometimes Parkinsonian-like symptoms. Studies have shown that both atypical and older antipsychoticsare associated with increased risk of death in elderly dementia patients. These drugs should not be used routinely, and if needed, the minimum dosage should be used for the minimum amount of time, under careful supervision of an experienced clinician.

Patients and caregivers should also be cautious of over the counter medicine containing diphenhydramine (Benadryl). Diphenhydramine is an antihistamine that tends to make people drowsy. It also has anticholinergic effects that may result in confusion and worsening cognition. Diphenhydramine is found in sleep aids such as Compoz, Nytol, Sominex, Unisom, and also in “night time” or “pm” version of popular pain relievers, cold and sinus remedies.

In essence, patients with Alzheimer’s disease are particularly vulnerable to side effects from various medications. It is best to consult with your doctors and pharmacists to learn about the benefits and potential adverse effects of any new treatment therapy, including seemingly benign over the counter remedies.

Source: Gaby T. Thai, M.D., 19 April 2011
http://www.alz.uci.edu/medications-and-patients-with-alzheimer%E2%8...

Stress and Its Influence on Alzheimer’s Disease

2011-11-23T05:28:00.016+08:00

Aging is an inevitable journey for everyone, and includes many obstacles and different paths to take. How we live our lives can have enormous impact on whether we grow old gracefully, or succumb along the way. Good physical health, through diet and exercise, will allow people to remain active well into their twilight years, but as lifespan increases it is also important to take care of and maintain brain health as well. Fortunately, it appears that what is good for the heart is also good for the brain, and thus by keeping active, both physically and mentally, and maintaining a healthy diet rich in omega 3 fatty acids, a person can have the best chance of aging successfully, and avoid both heart disease and brain disease.

The major brain disease of the elderly is Alzheimer’s disease. It affects 1 in 20 people aged 65 and over, and its incidence increases with age such that around half of people aged 85 and over have the disease. Alzheimer’s disease is a devastating disorder that robs a person of their memories and cognitive abilities, rendering them unable to recognize family members, or care for themselves. But what is it that causes Alzheimer’s disease? Why do some people develop Alzheimer’s disease and not others? By asking, and then understanding these questions, we, as scientists, can develop therapies and strategies to help people avoid developing the disease in old age.

Here within UCI MIND, we have devoted considerable resources to identifying the causes of Alzheimer’s disease, and finding ways to circumvent these causes. We have identified how the stress hormone cortisol can play a role in the development of Alzheimer’s disease. Cortisol is a steroid hormone that is produced in the adrenal gland in response to times of stress. In the short term, following a stressful experience, cortisol levels rapidly increase in the blood stream, and its presence is helpful – improving short-term memory formation and adapting the body’s physiology to deal with the situation effectively. However, long-term stress leads to prolonged elevated levels of cortisol within the blood stream, which can have serious deleterious effects.

It was found, over twenty years ago, that patients with Alzheimer’s disease had elevated levels of cortisol in their blood streams, compared to healthy patients. This elevation correlated with the degree of memory impairments that the patients had and appeared early on in the disease progression. We were interested in whether or not these early increases in circulating cortisol could be contributing to the development of Alzheimer’s disease, by leading to the pathologies that are found in the AD brain. It is the accumulation of sticky proteins in the brain, leading to a loss of neuronal function, which underlies the dementia and memory loss seen in Alzheimer’s disease. Typically 2 sticky proteins are present in the Alzheimer’s disease brain – the first is the amyloid-beta peptide(Ab), which stick together in between neurons and form the extracellular plaques. The second sticky protein is known as tau, which becomes modified in the Alzheimer’s disease brain causing it to stick together inside neurons and disrupting normal neuronal function. The net result of these sticky proteins is a cascade of events leading to widespread synaptic and neuronal loss in the brain, which causes the dementia and memory loss.

Relax! Avoid stress...

We showed that cells treated with cortisol produced dramatically larger amounts of this Ab peptide – which can accumulate to form the Ab plaques. In order to test whether increased cortisol could have a similar effect in animals and by extension people we turned to a genetically altered mouse, which had been engineered to develop Alzheimer’s disease pathology in its brain as it aged. We took young animals, before they were old enough to have Alzheimer’s disease pathology, and we injected them with a rodent equivalent of cortisol every day for 1 week. After just a single week we looked inside the brains of these animals and found that levels of both Ab peptide and tau protein were tremendously elevated. This showed us that increase in circulating cortisol in humans is able to increase the pathology present in the brain – and thus could make people develop Alzheimer’s disease faster.

So how can we use these findings to help people reduce their risk of developing Alzheimer’s disease in old age? Firstly, cortisol levels are increased by stress – a study has also shown that people with stressful lives are around 2-3 times more likely to develop Alzheimer’s disease than others. So avoiding stress is paramount. In addition, these results can be used by scientists to develop drugs to block either the production of cortisol, or to prevent its effects once it is produced. This could lead to a slowing of the disease if it proves successful.

Stress reduction, combined with a healthy lifestyle and diet will help people age successfully and avoid disease.

(Source:http://www.alz.uci.edu/stress-and-its-influence-on-alzheimer%e2%80%99s-disease/)

(SAT)10DEC11 Talk On "Laughter Yoga" & Exercise Session, Organized By ADFM KL-PJ Alzheimer's Caregivers Support Group

2011-11-22T14:37:00.009+08:00

Dear All,

Karen Sze Tho, Certified Laughter Yoga Teacher, will be conducting a Talk on “Laughter Yoga” and Exercise Session for our Caregivers and Members.

Date : Saturday, 10 December
Venue : ADFM PJ Daycare Centre. No. 6, Lorong 11/8E, Section 11, 46200 PJ
Time:

2:00pm : Registration
2:30pm : Introduction by CLY Teacher, Karen Sze Tho
2:50pm : Exercise Session
3:50pm : Sharing Session
4:10pm : Light Refreshments

Laughter Yoga was first introduced to Johor Bahru (JB) in 2008 and since then has been much sought after in Malaysia and Singapore.

Karen will give an introduction on understanding the basic concept, philosophy of Laughter Yoga and what happens in a LY session, techniques of how to laugh all by yourself and the Multiple Health Benefits.

Speaker’s Profile

Karen Sze Tho is a Certified Laughter Yoga Teacher (CLYT) trained by the Founder of the Laughter Yoga Movement, Dr . Madan Kataria in Bangalore, India in January 2010.

Karen's passion with LY started in 2001 when she saw an episode of LY on National Geographic on TV. It was only in 2010 that she had the opportunity to learn from the Master.

Since her Certification, Karen has conducted numerous LY sessions with senior citizens, training academies, children’s homes, companies and at events.

Confirm your registration (on first- come first-served basis):
1. Email jenny@adfm.org.my / Tel: 03-7956 2008/7958 3008 / SMS 016- 608 2513 / Fax 03-7960 8482
2. Christine at 03 - 2260 3158.

Come, have fun and experience this simple, easy & light-hearted exercise

JOIN THE ADFM NATIONAL ALZHEIMER’S CAREGIVERS NETWORK
Your National Platform for The Caregivers Community
SIGN UP, Click at : “http://admalaysia.ning.com/main/authorization/signUp”
(If you do not have an Email Account, contact us at Tel: 03-7956 2008 / 7968 3008)

Advanced-Stage Dementia & Hospice Care

2011-11-15T20:06:00.004+08:00

CBS News - Gertrude Buckley was a beauty with brains - one of Milwaukee's first female real estate brokers. But around her 80th birthday, her family began noticing odd behavior.

"Her checkbook was a mess. She wrote checks for very much the wrong amount," said Paula Tishel, Buckley's daughter. "She completely denied that she had any memory loss. 'That's ridiculous,' is what she would say."

Buckley is now 93 years old, with advanced dementia. A controversial new study finds her illness is as deadly as cancer and, therefore, its victims should be offered hospice care to spare them from futile and frightening procedures, reports CBS News medical correspondent Jon LaPook.

"Far too many patients experienced distressing symptoms like pain and shortness of breath and received burdensome interventions of questionable benefit in the final days of life," Dr. Susan Mitchell said.

But how do you know when someone is in the final days of life?

Researchers found patients with late-stage dementia - those who speak fewer than six words at a time and are completely dependent - lived on average only 16 months. And about 40 percent were in pain.

Advanced dementia has the same poor prognosis as terminal cancer. But only about 18 percent of family members say this has been explained to them by doctors.

Those who did were far less likely to allow extraordinary measures like feeding tubes and emergency room visits.

"If you're someone who doesn't understand who is doing this or why they're doing it, it's going to feel almost like an assault," said Dr. Greg Sachs of the Indiana University School of Medicine's Center for Aging Research, said of the medical procedures conducted on dementia patients.

Sachs watched his own grandmother suffer through aggressive treatments right up until she died.

He's among a growing number of doctors who advocate hospice care to comfort patients such as Gertrude Buckley. Medicare has covered hospice care since the 1990s but is used on only one in 10 patients with advanced dementia.

"Certainly I'm not advocating sending grandma off on an ice floe," Sachs said. "It's a misconception people either get aggressive care or they get neglected or they get put to death. People actually have a right to aggressive palliative care. They need someone who is responsive to their pain."

Because Buckley left no advanced care instructions, her daughter has been left guessing about her mother's wishes.

"I know that she wouldn't want to be in pain, nobody would. I don't want her to be frightened. I opted not to do anything that was uncomfortable to her but just to make sure that she was really well taken care of and stimulated and comfortable."

Experts stress the goal of hospice care for patients with advanced dementia is hot to hasten their death, it's to make their last days as comfortable as possible.

Watch Video - Advance Dementia-Managing the Burden ...

(Source: Latest Alzheimer's Weekly and Dementia Weekly Newsletter)

The New Alzheimer's Tangles: Tau, Neurofilaments and Vimentin

2011-11-14T20:18:00.004+08:00

Scientists from the National Institutes of Health in the United States have made an important discovery that should forever change the scope and direction of Alzheimer's research. Specifically, they have discovered that the protein tangles which are a hallmark of the disease involve at least three different proteins rather than just one. The discovery of these additional proteins, called neurofilaments and vimentin, should help scientists better understand the biology and progression of the disease as well as provide additional drug discovery targets. This discovery was published in the November 2011 issue of the FASEB Journal.

"Since neurofilaments are the predominant protein in nerve cells, our study suggests that we should refocus our research on the biology of these filamentous proteins in an effort to understand how they are normally regulated and deregulated in response to human aging," said Harish C. Pant, Ph.D., a senior researcher involved in the work from the Cytoskeletal Regulatory Protein Section of the Laboratory of Neurochemistry at the National Institute of Neurological Disorders and Stroke at the National Institutes of Health in Bethesda, Maryland.

To make their discovery, Pant and colleagues identified normal and abnormal proteins present in autopsy samples of the brains of Alzheimer's disease victims. Then they isolated and purified the tangles (which are knots of abnormally aggregated filaments that fill and compromise nerve cells) from the autopsy samples and compared their protein composition to age- and post mortem-matched samples of brains from patients who died of other causes, such as accidents. Through a combination of improved instrumentation and informatics, it was possible to resolve the mixture of proteins successfully and identify the novel Alzheimer's disease proteins. Previous research suggested that only one protein, called "tau," is present in these tangles.

"This is a breakthrough of great importance: tau is not the only target," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "Before this discovery, we approached these tangles as if they were woven of one piece of string. Now we know that there are at least three proteins involved, we're much closer to untangling the Alzheimer's web. Without question, discoveries like this bring us closer than ever to advanced Alzheimer's treatments, and it is a good example of why NIH funding is among the best investments our nation can make toward improving health and well being.

(Source: Latest Alzheimer's Weekly and Dementia Weekly Newsletter)