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Calorie restriction may prevent Alzheimer's 

Public release date: 14-Jun-2006
Contact: Mount Sinai Press Office
NewsMedia@mssm.edu
212-241-9200
The Mount Sinai Hospital / Mount Sinai School of Medicine
http://www.eurekalert.org/pub_releases/2006-06/tmsh-crm061406.php

Artricle:
Calorie restriction may prevent Alzheimer's through promotion of longevity program in the brain
For the first time researchers show how restricting caloric intake triggers activity in the brain associated with longevity
New York, New York – A recent study directed by Mount Sinai School of Medicine suggests that experimental dietary regimens might calm or even reverse symptoms of Alzheimer's Disease (AD). The study, which appears in the July 2006 issue of the Journal of Biological Chemistry, is the first to show that restricting caloric intake, specifically carbohydrates, may prevent AD by triggering activity in the brain associated with longevity.

"Both clinical and epidemiological evidence suggests that modification of lifestyle factors such as nutrition may prove crucial to Alzheimer's Disease management," says Giulio Maria Pasinetti, M.D., Ph.D., Professor of Psychiatry and Neuroscience, Director of the Neuroinflammation Research Center at Mount Sinai School of Medicine and lead author of the study. "This research, however, is the first to show a connection between nutrition and Alzheimer's Disease neuropathy by defining mechanistic pathways in the brain and scrutinizing biochemical functions. We hope these findings further unlock the mystery of Alzheimer's and bring hope to the millions of Americans suffering from this disease."

Alzheimer's Disease is a rapidly growing public health concern with potentially devastating effects. An estimated 4.5 million Americans have Alzheimer's Disease and the number of Americans with Alzheimer's has more than doubled since 1980. Presently, there are no known cures or effective preventive strategies. While genetic factors are relevant in early-onset cases, they appear to play less of a role in late-onset-sporadic AD cases, the most common form of AD.

Longevity Program in the Brain
People with AD exhibit elevated levels of beta-amyloid peptides that cause plaque buildup in the brain (the main characteristic of AD). Beta-amyloid peptides activate SIRT1, a member of a broad family of proteins known as sirtuins which influence a variety of functions including metabolism and aging.

Dr. Pasinetti and colleagues used an experimental mouse model to demonstrate that beta-amyloid peptides in the brain can be reduced by subjecting the mice to dietary caloric restriction, primarily based on low carbohydrate food. Conversely, a high caloric intake based on saturated fat was shown to increase levels of beta-amyloid peptides.

This study is the first to suggest that caloric restriction through promotion of SIRT1 (a molecule associated with brain longevity) may initiate a cascade of events like the activation of alpha-secretase which can prevent AD amyloid neuropathology. Since alpha-secretase is known also to inhibit the generation of beta-amyloid peptides in the AD affected brain, the study demonstrates a mechanism by which dietary caloric restriction might benefit AD. Most remarkably, the study finds that a high caloric intake based on saturated fat promotes AD type beta-amyloidosis, while caloric restriction based on reduced carbohydrate intake is able to prevent it.

Implications
Among lifestyle factors influencing AD, recent studies strongly support the evidence that caloric intake may play a role in the relative risk for AD clinical dementia. Most importantly, as mechanistic pathways are defined and their biochemical functions scrutinized, the evidence supporting a direct link between nutrition and AD neuropathology continues to grow. 

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New study supports anti-aging benefits of cutting calories
Posted on Fri, Jun. 02, 2006
By Tina Hesman Saey
KNIGHT RIDDER NEWS SERVICE

ST. LOUIS - Washington University researchers have found another reason that cutting calories lengthens life.

A recent study reported that eating a high-nutrition low-calorie diet could reverse signs of aging in the heart.

Now scientists, led by Dr. Luigi Fontana, have discovered that cutting calories also can cut levels of body chemicals associated with aging.

Fontana and his colleagues studied three groups of 28 people each. The first group consisted of people on calorie-restricted diets. The people built highly individualized diets from fruits, vegetables, nuts, lean proteins, dairy products and whole grains. Calorie consumption ranged from 1,112 calories per day to 2,260 calories per day with an average intake of 1,779 calories per day. People in the group had followed the restricted diet for an average of six years but were sedentary.

The second group consisted of endurance runners who logged an average of 48 miles per week. The runners ate an average of 2,811 calories each day. Both the exercisers and dieters had very low body fat.

A third group consisted of sedentary people who ate a standard Western diet. The sedentary group consumed, on average, 2,433 calories in a day.

All of the groups were composed of healthy non-smokers who had stable weights and weren't taking medicines or dietary supplements that might interfere with the results.

The researchers reported that the calorie-cutters, but not the runners or non-dieters, had lower levels of a thyroid hormone called T3 in their blood. The hormone is associated with metabolism, body temperature and the production of free-radicals, chemicals linked to cancer and aging. The calorie restriction group also had lower levels of an inflammatory protein called tumor necrosis factor alpha (TNF alpha.) Inflammation is thought to cause damage that promotes aging.

The fact that the runners had low body fat similar to the calorie restriction group, but didn't have lower levels of aging-related chemicals, means that just being lean isn't enough to fight aging, Fontana said. Only lowering energy intake seems to change the factors that contribute to aging.

The results of the new study were reported last week in the online edition of the Journal of Clinical Endocrinology and Metabolism.

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