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Alzheimer’s Risk Falls With Activity

admin — Sat, 12 May 2012 12:49:43 +0000

Intensity matters, but it isn’t just about exercise.

Cleaning house and doing yard-work are taking on new importance. A higher level of physical activity – not just exercising – is linked to a reduced risk of developing Alzheimer’s disease even in people over 80, suggests research published Wednesday in the journal Neurology.

Protective activities washing dishes, cooking, cleaning, gardening – even playing cards. People who scored in the bottom 10% of physical activity were more than twice as likely to develop Alzheimer’s. Study participants did not have dementia at the start of the four-year study, which is part of the ongoing Memory and Aging Project at Rush University Medical Center in Chicago.

“The implication of this study is really outstanding,” says physician Aron Buchman, the lead author. “Exercise is good, without a doubt, but this study is about more than exercise. Older people who might not be able to exercise can tailor activities that are right for them.”

There is no cure or drug to delay onset of Alzheimer’s, which affects about 5 million in the USA; numbers are expected to triple as Baby Boomers get older. Aging is the main risk factor.

During the study, 71 of the 716 study participants developed Alzheimer’s. Study author’s say this is the first study to use an objective measurement of all physical activity in addition to self-reports. Participants wore and actigraph on their wrists to assess levels of activity.

Their mean score was 3.3 hours a week. Exercise intensity also mattered; those in the bottom 10% for intensity of physical activity were almost three times as likely to develop Alzheimer’s.

The study is the latest evidence that physical activity, even in later years, aids in delaying Alzheimer’s. The study did not attempt to measure which activities were most helpful.

“We’ve known that muscle activity generates neurons in the brain, but this study gives us additional motivation,” says physician Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City, who was not associated with the study. “It shows you don’t have to go to the gym. Older people very often don’t want to do that.”

Results did not vary by age, sex or education. The authors also looked at chronic health and genetic factors. Among the findings:

Body mass index, depressive symptoms or vascular risk factors did not change the association between activities and risk.
Having the gene APOE4, which puts people at higher risk for developing Alzheimer’s, did not affect the results.

Alzheimer’s develops for years prior to symptoms occurring, Kennedy notes. The authors tried to control for that possibility by administering baseline cognitive tests.

“This is an important message for society, as the largest growing segment of our population is old people,” Buchman says. “We need to be encouraging physical activities even in very old individuals, even if their health doesn’t allow them to take part in fitness programs.”

In an accompanying editorial, the authors cite physical activity as a promising, low-cost, accessible and safe means to prevent Alzheimer’s.

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New Fronts on the Battle Against Alzheimer’s

admin — Thu, 06 Oct 2011 01:19:24 +0000

In March, the Alzheimer’s Association released its annual facts and figures on Alzheimer disease (AD). The analysis revealed some sobering numbers. AD remains the number one cause of dementia among the elderly. An estimated 5.4 million Americans suffer from the disease, and it has become the sixth leading cause of death. More importantly, among the top 10 causes of death, AD remains the only one without truly effective treatment options.

Also released this year in Alzheimer and Dementia were new diagnostic criteria and guidelines for AD, which update the diagnosis and expand the condition to those that have mild cognitive impairment (MCI) due to AD. This recognition of an earlier condition agrees with the growing evidence that AD may begin many years, even decades, before clinical signs of dementia are evident.

Also included in the new criteria is a framework for the eventual addition of biomarkers in the diagnosis.

These biomarkers include measurements of structural changes in the brain, such as reduced hippocampal volume and medial temporal atrophy, as well as CSF measurements of the prime suspects in AD, A?, and tau.

Ongoing Efforts

While A? and tau are each hallmarks of the disease, they also represent the major front in the fight against AD. Johnson & Johnson, Pfizer, and Elan are developing a humanized antibody to beta-amyloid, called bapineuzumab, that is meant to clear A? from the brain.

A study published in Lancet Neurology in 2010 by Rinne and co-authors demonstrated that treatment with bapineuzumab reduced levels of A? in the brain. Encouragingly, recent data suggests that improvement in cognition may be occurring with treatment. However, positive effects may be limited to noncarriers of the primary genetic risk factor for AD known as APOE4.

Two other immunological approaches to A? are also in the works. Baxter is developing its infused immunoglobulin product, Gammagard, for AD, and Eli Lilly is developing its own humanized antibody to A? called solanezumab. Each of these products has reported modest success in delaying cognitive decline in AD. Unfortunately, none of these immunological approaches have produced the type of results that the field would like to see.

Another highly anticipated class of compounds are gamma secretase inhibitors, which reduce the activity of the enzyme complex that cleaves the amyloid precursor protein and thereby lowers A? production. One of the first gamma secretase inhibitors to undergo extensive clinical testing, Flurizan, was developed by Myriad Genetics. Myriad ran an extensive Phase III trial in the U.S. with Flurizan, yet the study missed all its clinical endpoints.

Eli Lilly advanced another well-studied gamma secretase inhibitor called semagacestat into the clinic. Unfortunately, the semagacestat trial was halted when it was found that patients in the treatment group were deteriorating faster than those in the control group.

Bristol-Myers Squibb has also developed a gamma secretase inhibitor called BMS-708163, which was studied in 209 mild-to-moderate AD participants and met its primary objective of identifying safe and tolerable doses. No improvements in cognitive outcomes were seen, however.

One of the most promising new therapies for AD in recent memory was the compound latrepirdine, more commonly known as dimebon. In a Phase II study published in The Lancet in 2008, dimebon demonstrated improvements across the board in cognitive tests, raising expectation that a truly effective therapy was on hand. However, a replication of the study in a larger population did not yield positive results.

With the disappointing results of recent drug trials, it is vital to open new avenues to tackle AD. A large study on supplementing the diet with the omega-3 fatty acid docosahexanenoic acid (DHA) was completed in 2010 and reported in the Journal of the American Medical Association.

This comprehensive study examined 402 individuals in a placebo-controlled, double-blind, 18-month study to measure the effects of 2 grams a day of DHA on cognitive performance. Unfortunately, supplementation with DHA did not improve cognitive performance, nor did it slow progression relative to placebo.

A similar approach examined the effects of a medical food comprising ingredients designed to provide the building blocks for synapses, including uridine, omega-3 polyunsaturated fatty acids, and choline. This combination had shown impressive preclinical results.

A proof-of-concept study published in Alzheimer’s and Dementia in 2010 examined the effects among 225 participants in 12 weeks of therapy compared to placebo in a double-blind, placebo-controlled study. Encouraging results were seen among a predefined subgroup of mild AD patients, prompting additional studies currently under way.

Another avenue for intervention is the well-characterized decreased cerebral metabolism that occurs in AD. This glucose hypometabolism is one of the earliest markers of the disease and interventions in this process have met with some success.

In a study published in Neurobiology of Aging, Craft and co-authors found that nasal insulin could result in rapid increase in cognition in AD patients. Similarly, in a study of 511 mild to moderate AD subjects published in the Journal of Pharmacogenomics in 2006, Risner and co-authors found that administration of the insulin-sensitizing agent rosiglitazone improved cognitive scores. Unfortunately, larger studies did not repeat the improvements seen with rosiglitazone.

Another approach to addressing hypometabolism involves the induction of ketosis. Ketosis is defined as the presence of ketone bodies in the blood. Ketone bodies are a normal product of human physiology and are produced under conditions of low glucose availability, such as during fasting or the use of ketogenic diets. Ketone bodies are one of the few substrates the brain can use for energy.

Two recent studies examined the induction of ketosis in AD. Both reports utilized medium chain triglycerides (MCTs) to induce ketosis. Instead of being stored as fat, MCTs undergo obligate oxidation in the liver and can induce ketosis even in the presence of a normal diet.

Amidst the failures have been a number of positives that continue to propel the field forward. Development of new treatments remains a top priority for industry, advocacy associations, and government agencies.

http://www.genengnews.com/gen-articles/new-fronts-on-the-battle-against-alzheimer-s/3816/

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History of Head Trauma in Alzheimer's Disease

admin — Wed, 18 Mar 2009 04:24:12 +0000

It turns out generally that whether a history of head trauma or injury is a cause of Alzheimer’s disease of the symptoms of Alzheimer’s disease is not certain or indeed uncertain by itself.

It can be pointed out that some published studies of repute suggest that head trauma that results in what may or should be considered a loss of consciousness is a definite risk factor and factors into the risks of a patient developing Alzheimer’s disease.

Thus people who expose themselves to repeated head trauma or injury , such as you might find in the classic cases of boxers such as Muhammed Ali, who developed serious Parkinson’s disease – perhaps as a result of his boxing career, or football players can be said to be , as a result , at a higher risk of developing Alzheimer’s disease as opposed to if they had not followed their chosen career path or paths. Regardless of whether or not actual Alzheimer’s disease progresses as a result of the specific person’s health and mental and memory cognitive skill levels- many such people who are continually exposed to head trauma and head trauma injuries do go later to more often than the general population , have incidences of difficulties of memory , concentration, speech and other brain function difficulties higher than the general population overall .

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Misconceptions and Misunderstandings Concerning Alzheimer's Disease

admin — Mon, 26 Jan 2009 15:09:05 +0000

It can be said that there are no shortage of misconceptions that are commonly held in relation to Alzheimer’s Disease and dementia in general.

Among these are :

- that people get Alzheimer’s Disease in their forties or fifties

- that dementia is the same as senility or aging

- that if your mother developed Alzheimer’s Disease in her eighties, you have a close to 95 % percent chance of getting it as well

- Alzheimer’s brain changes may start years or decades before memory problems begin or become fully apparent

- specialists can tell up to 90 % accuracy whether or not someone has Alzheimer’s

- a depressed mood or vitamin deficiency can impair one’s memory

- there is no approved medication or medications for treating Alzheimer’s symptoms. The only option , as the misinformed or those with misconceptions are for “experimental drugs”

- high blood pressure or obesity may increase one risk of dementia. “You eat too much” may be the refrain from dietitian types who see all health evils as a result of overeating

- being socially involved and keeping one’s mind active may postpone Alzheimer’s

- that all clinical research studies involve taking risky experimental drugs.

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