Sunday, 19 February 2012

Dear Caregivers/Members,

ADFM National Caregivers Network is holding a Presentation on:

Date : Saturday, 24 March 2012
Time : 2:00pm - 5:00pm
Venue : ADFM PJ Daycare Centre, 6, Lorong 11/8E, Section 11, 46200 PJ
1:30pm  :  Registration of Attendance
2:00pm  :  Welcome Address by Chairman, Datuk Dr Yim Khai Kee
4:10pm  :  Q & A Session
4:40pm  :  Light refreshments

1.  “Care Giving OR Giver” are honourable phrase.  Do we understand what it means ??????

In his presentation, Willie Kwa hopes to explore the understanding of care giving and issues surrounding how care is action that is, direct care intervention, non medical therapies, etc, etc.

2.  “Communication” is a key action associated in any given life interaction, more so with someone who has DEMENTIA.

The goal in all communications with a person who has Alzheimer’s disease should be to connect with the person in a positive, constructive, effective way.

Mr Willie Kwa from UK is Malaysian born and bred. A distance Carer for a loving Mom who had Vascular Dementia.  Willie, a qualified Mental Health Practitioner,  has been professionally delivering care within the National Health Services (NHS) for over 40 years and retired in 2007.  Since retirement, Willie has been working as locum for care agency delivering care at various private Dementia Care Home.  35 years of his professional working life were spent with people who have Dementia.

1.  Compulsory registration (first come first serve basis) due limited places. 

2.  Email attached Registration Form to : / Fax: 03-7960 8482  OR  SMS Jenny at 016-608 2513 with full name/s and Tel/mobile contact if you do not have internet access.

For further information, please call Tel: 03-7956 2008/016–608 2513.

 National Platform for The Caregivers Community

From:  ADFM National Caregivers Network
February 2012

Friday, 17 February 2012

The Agony of Isolation and Family Caregiving : An Alzheimer’s Tragedy

The pain of isolation for the family caregiver increases exponentially as Alzheimer’s advances. On a scale of one to ten, ten being the highest, isolation must be at the top of the list.  As a woman once wrote and providing care for her aging father, “With Easter tomorrow I’m feeling forgotten by people around me and it’s making me feel blue”. It is estimated that millions of baby boomers will be diagnosed with Alzheimer’s within the next decade. For every one diagnosed with Alzheimer’s, a primary family caregiver is becoming responsible for an average of four to six years, and perhaps as long as 20 years, after the diagnosis of Alzheimer’s according to the Alzheimer’s Association (

When I became a family caregiver for my husband 10 years ago, I was focusing on creating systems to provide the best care possible, safety was top of my to-do list and living two lives at once (taking care of all his needs, thoughts and feelings along with mine) required a shift in perspective. By the time I felt established as a family caregiver, I noticed everyone around me had disappeared, my social activities were non-existent because there was no time after devoting 24/7 to my husband, and I was feeling extremely isolated in this world - not even able to share thoughts and feelings with my husband for fear of confusing him even more.

Words that come to mind when pondering on this feeling of isolation are: sadness, mourning, loss, fear, and despair. Although I have a background as a mental health counselor and know the importance of combatting isolation, it became obvious to me that devoting 24/7 on family caregiving duties and responsibilities became overwhelming for me. Such a schedule did not leave any room for reaching out and getting in touch with others. There was no energy or desire for engaging in activities outside my home. I was simply physically and emotionally exhausted, and the expression “can’t see the forest for the trees” seems fitting.

What I found most helpful was an occasional visit from my sister and her husband who were able to see physical and emotional changes in me because they know me well. My sister did not hesitate to “drag” me to a restaurant when I was having a professional caregiver for a few hours for respite. She also did not hesitate to let me know when it was time to place my husband in long-term care because he no longer was able to walk unassisted and all the lifting on him meant my own body was starting to fail me. Did you know there is research showing that an individual living at home does not live any longer than living in long-term care? 

It has been almost two years since my husband moved into long-term care but I am still recovering from being a family caregiver. I must have slept at least four months, sleeping in bed or a recliner (any time of day or night) in those months. Now that I have more time and can get out and socialize, I have trouble finding avenues where I might make new friends. Creating an exercise program that benefits me has not been as easy as I thought, but I’m getting there. Results of this isolation includes, but is not limited to, premature aging, depression, exhaustion, high blood pressure and even despair in many family caregivers. They often feel they have been abandoned by family, friends and even their close neighbors. In reality it is often the profound emotional and physical changes in them that create such feelings, whether these feelings are real or imagined.


Treat caregiving as though you were a profession and take regular breaks. Keeping a 24/7 schedule is a recipe for disaster. My advice is to find in-home help or support early after becoming a family caregiver. Start from the first day to look for that professional help and get out of the house while that individual is there with your loved one. Let family members know that you need them in your life now more than ever and visit with them more often. In order to visit relatives avail yourself of respite care in long-term care where you know there is a team of professional caregivers to cover your time away from home. Take time to pause in order to be able to ask for what you want from others.

Know the four stages a family caregiver will experience ( and actively take steps to manage each stage better:

1.      Early Stage: Basic care
2.      Middle Stage: Intermediate care
3.      Late Stage: Advanced care
4.      Bereavement Stage: End-of-life care

If you care for a parent or relative outside your home, consider moving them into your home to minimize travel time on your part. Get financial advice early in order to make proper budgetary adjustments so the financial stress is reduced and it is possible to make ends meet. On holidays and special occasions treat yourself so that you feel special. Finally, you may want to consider the services of a professional Alzheimer’s coach to provide the guidance and support you need through this challenging period in your life.

About the Author:
Ethelle G. Lord has her Doctorate of Management in Organizational Leadership from the University of Phoenix (2010). Dr. Lord is An Adjunct Professor of Business, Author and Professional Alzheimer’s Coach. She has her own coaching business at Remembering for You (dot) Com and Teamwork Coaching (dot) Com. From 1992-1996  she had a private practice in mental health counseling; in the late 80s she was a paralegal for Legal Services for the Elderly and from 1992-1996 she was a two-term President of the Maine Gerontological Society of Maine. Ethelle is married to Maj. Larry S. Potter, USAF Retired. They live in Maine. 
Visit : and contact the author at

Tuesday, 14 February 2012


(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

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.

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

Monday, 13 February 2012

Hope For Early Alzheimer's Test In Spinal Fluid

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

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:
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

(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.


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.

Thursday, 2 February 2012

Metals Could Be A Potential Target In Fighting Alazheimer's

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.

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.

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.

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.

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