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Alzheimer's, Dementia, Mental Health
Alzheimer's May be Prevented by Less
Carbohydrates, Triggering Longevity Activity in Brain
Direct link between
nutrition and Alzheimer's continues to grow
June 15, 2006 – A recent study is the first to show
that restricting caloric intake, specifically carbohydrates, may prevent
Alzheimer's Disease by triggering activity in the brain associated with
longevity.
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Alzheimer's & Dementia |
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The study, directed by Mount Sinai School of
Medicine, appears in the July 2006 issue of the Journal of Biological
Chemistry. It suggests that experimental dietary programs might calm or
even reverse symptoms of AD.
"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 (disease
of nervous system) 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.
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Hormone that
Turns Off Hunger Also Improves Memory |
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Experiment worked best in older mice with
Alzheimer's
June 15, 2006 – A recent research report has
found a connection between memory problems and obesity. The
scientists were investigating why obese patients with diabetes
also often have long-term memory problems. They found that mice
navigated a maze better after they received leptin, a hormone
secreted by fat cells that warns people to stop eating.
"In obese people, it doesn't cross into the brain
to help regulate appetite," says Susan A. Farr, Ph.D., principal
investigator and associate research professor in the division of
geriatric medicine at Saint Louis University School of Medicine.
Mice with elevated levels of amyloid-beta
protein, the brain plaques believed to cause Alzheimer's
disease, and impaired learning and memory were "super sensitive"
to leptin, Farr adds.
"In the older mice that have Alzheimer's disease,
leptin worked even better and at a lower dose than it did in
younger mice."
"We've now found leptin affects the brain in
other ways, compromising learning and memory. Low levels of
leptin also could be related to cognitive deficits in disorders
like type two diabetes."
"We found that this drug affected the processes
going into the brain," says Farr, who also is a researcher at
Veterans Affairs Medical Center in St. Louis. "The mice that got
the drug at the appropriate dose had improved learning and
long-term memory."
The research is published in this month's
Peptides.
Established in 1836, Saint Louis University
School of Medicine School is a pioneer in geriatric medicine.
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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.
About information source:
Mount Sinai School of Medicine
Located in Manhattan, Mount Sinai School of Medicine is internationally
recognized for ground-breaking clinical and basic-science research, and
innovative approaches to medical education. Through the Mount Sinai
Graduate School of Biological Sciences, Mount Sinai trains biomedical
researchers with an emphasis on the rapid translation of discoveries of
basic research into new techniques for fighting disease.
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