Rays of Hope in the Fight Against the Spread of Alzheimer’s

Nearly five million Americans are living with Alzheimer's disease, according to the Alzheimer's Association. Experts predict the number will reach 16 million by 2050.

Scientists are working to prevent that projection from becoming a reality - or at least trying to find a treatment that will ease the effects of the debilitating, memory-robbing disease. In the past few months, Alzheimer's researchers have made notable progress that could one day lead to improved treatments for the disease or even methods of preventing it. Nonetheless for many of us who have loved ones with Alzheimer’s, breakthroughs in Alzheimer’s research have been slow to show promise.

"Science usually works in a slow, deliberate fashion," says Peter V. Rabins, M.P.H., M.D., director of the Division of Geriatric Psychiatry & Neuropsychiatry at Johns Hopkins. "That is a strength, because it can prevent mistakes such as exposing people to drugs that don't work and that have serious side effects. But it leads to frustration in people when they or their loved ones have the disease being studied."

Here’s a brief overview of a few recent studies you’ll want to follow in the months ahead …

• Biomarkers in the cerebrospinal fluid in brains and spinal cords of people with mild cognitive impairment, the precursor to Alzheimer's disease, can predict Alzheimer's up to 10 years before symptoms appear. This finding can open the door to the development of new treatments that may stop the disease's progression early on.

• People who have amnestic mild cognitive impairment (aMCI), a condition in which the only difficulty is with memory, appear to be at increased risk for developing Alzheimer's. Patients with aMCI have more memory loss than normal for their age, but their symptoms aren't as severe as Alzheimer's are. A simple questionnaire can help identify people with aMCI, thereby allowing them to begin Alzheimer's diagnostic testing and treatment sooner rather than later. 

• Inherited early-onset Alzheimer's disease may be more closely related to late-onset Alzheimer's than previously thought. Scientists have found similar gene mutations in both forms, leading some experts to believe that each may have the same causes. Detection of the gene may give doctors a new tool to help determine the correct treatment approach in current Alzheimer's patients.

• People who participate in cognitively stimulating activities like reading, writing, playing games and solving puzzles throughout their lives tend to have fewer deposits of beta-amyloid in their brains as they age. Researchers have long suspected that keeping the brain active helps ward off Alzheimer's, but this is the first time they've been able to identify an underlying biological link.

(Source:  John Hopkins Health Alert, Posted in Memory on May 28, 2012)

Study Finds: Having Purpose In Life Helps Fight Alzheimer's

New research suggests that having a purpose in life may help protect people from health issues such as Alzheimer's and other cognitive problems. In this preliminary study, scientists defined "purpose in life" as intentionally engaging in behaviors that one thinks are important.

Research done by Memory and Aging Project at Rush offers hope in fight against disease. 

Charlotte Morrison loves to walk, practice tai chi and paint with watercolors.  Morrison, 83, finds meaning in helping others who live with her in the Bethlehem Woods Retirement Community in LaGrange Park to express themselves. "Every morning, I ask myself, 'How can I help someone today?' My purpose in life is to help people," she said.

Morrison worked with developmentally disabled children and adults for 32 years, then cared for her husband for seven years before he died.

After Alzheimer's disease took his life, she joined the Memory and Aging Project at Rush University Medical Center, about 3 1/2 years ago. "I will do anything to help anyone figure out Alzheimer's. Now research is coming up with real results, finding ways of helping people live better with Alzheimer's. It's an honor to be part of something like this," Morrison said.

Some of this research, including a study published in the Archives of General Psychiatry's May issue, has found that having a purpose in life can help protect individuals from health problems, including Alzheimer's disease and other cognitive disorders. The term "purpose in life" is defined as the tendency to be intentional, to engage in behaviors that one wants to engage in and thinks are important, said lead investigator Patricia A. Boyle, a neuropsychologist with the Rush Alzheimer's Disease Center and associate professor in the Department of Behavioral Sciences.

"(The research) is exciting. It suggests possible behaviors that everyone can strive toward and that promote cognitive health. People are asking what they can do to prevent Alzheimer's, to maintain cognitive function. Find things that are meaningful and that help you feel life is purposeful," Boyle said.

Alzheimer's disease is the sixth-leading cause of death in the United States, with 1 in 8 older adults, and 5.4 million individuals, suffering from it, according to the Alzheimer's Association. Symptoms of Alzheimer's disease include loss of memory and thinking ability and functional changes, including reducing the ability to care for oneself.

Boyle and her colleagues looked at information from 246 of the more than 1,500 older individuals enrolled in the Rush Memory and Aging Project, which began in 1997. It studies chronic aging conditions among those living in the Chicago area. For up to about a decade, participants had yearly clinical evaluations, with neurological and cognitive testing.

Participants tended to be older, with an average age of about 80, and began the study without showing signs of Alzheimer's disease. Once a year, they were asked to rate themselves on the answers to certain questions, including how much meaning they derived from life's activities and whether they were goal-directed or purposeful.

"We found that for two people with a similar amount of Alzheimer's changes, the one with higher purpose in life did much better with cognitive function over time," Boyle said.

After the participants died, brain autopsies were performed on them. The researchers then looked at the plaques and tangles that had formed in their brains. Plaques and tangles are protein deposits associated with Alzheimer's disease. "They prevent brain cells from communicating effectively with each other," Boyle said.

"There is increasing evidence that almost everyone has some amount of plaques and tangles," she said.

With this information in mind, the idea becomes helping people to cope and still do well, perhaps by developing a purpose, Boyle said.

"Purpose in life is something everyone can work toward," she said.

It is part of an overall sense of well-being, including contributing to society, being a productive person, having goals and a knowledge of what's important to you, working toward those goals and contributing to the world, Boyle said.

The daily challenges one faces, including working to pay the bills, can make it difficult to maintain a focus on how people are spending their "most important resource — time," she said.

"I recommend that people think of their priorities. Think of what's important and meaningful to you, and move in that direction," Boyle said.

These activities could include spending time with family, and, perhaps doing a different kind of work. "These bring a sense of wellness that is protective. Studies are showing that this promotes health," she said.

Morrison said her work at Bethlehem Woods as an advocate is consistent both with her earlier work as a teacher for the developmentally disabled and her work with Alzheimer's research.

"I want everybody's grandchildren to not have Alzheimer's," she said. "I think that people in general know people who've had Alzheimer's. We are hoping that it's something that can be cured. I think they are getting on the right track."

(Source:  Alzheimer's Association - Chicago Tribune , 23 May 2012 By Jessica Tobacman)

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.

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

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:

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)

Advice to Keep Dementia at Bay

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)

Prevention Tip - Exercise Against Alzheimer's ...

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)

Breakthrough Closer for Alzheimer's Treatment After Vaccine Success

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)

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

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

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/)

Brain Exercises Versus Body Workouts In Preventing Dementia - Mental Gymnastics OR Physical Exercise?

Dear Caregivers / Members,

One of the posts on Preventing Tip of the Week from the latest Alzheimer's Weekly and Dementia Weekly Newsletter.

Read on ...

Brain Exercises Versus Body Workouts In Preventing Dementia -
Mental Gymnastics OR Physical Exercise?

Only one in ten people realize that taking regular exercise is one of the best ways to reduce their risk of developing dementia, according to a survey commissioned by Alzheimer’s Society and Bupa.

This is despite the fact research has shown that regular exercise can reduce your risk of dementia by up to a third.

Over a quarter (28%) of people believed brain training and crosswords to be the best way to reduce the risk of developing dementia, despite the jury still being out on whether this can be effective.

Dr. Anne Corbett, The Alzheimer's Society's Research Manager, said:
'This research shows that many people don't realize physical activity can have a real impact in determining whether you develop dementia. Along with moderating alcohol intake, maintaining a regular weight and not smoking, taking regular exercise can actually reduce your dementia risk by up to a third.'

Exercising can not only reduce a person's risk of developing dementia, but can also prevent other diseases related to lifestyle.

To "put their money where their mouth is," The Alzheimer's Society works with the Bupa organization to put together an impressive marathon. 3,500 people take part in the Bupa Great North Run to support The Alzheimer's Society, Bupa's nominated charity for a third consecutive year.

Dr. Graham Stokes, Bupa's Director of Dementia Care said:

'Lots of people believe that dementia is an inevitable part of old age - that's not the case at all and there's lots people can do to reduce their risk. Just 30 minutes of physical activity, five times a week will help reduce your risk of not only dementia, but also heart disease and diabetes. It doesn't have to be a vigorous workout - you can find ways to fit being active into your daily routine, such as walking, gardening or swimming.

If you're up for a challenge, supporting the Alzheimer's charities in a Bupa Great Run means you can get fit, help reduce your risk of dementia and raise money for a very worthwhile cause. As the UK's leading provider of dementia care, we're very pleased to be supporting Alzheimer's Society and Alzheimer Scotland for a third year.'

Over 19,000 people have taken part in a Bupa Great Run for Alzheimer's Society in the last two years, raising over £2 million. The aim is to raise over £3.5 million by the end of the year.

More importantly, it's a great way to prevent dementias such as Alzheimer's.

(Source: Alzheimer's Weekly & Dementia Weekly Newsletter)