X-Message-Number: 26326
Date: Sun, 12 Jun 2005 22:30:02 -0700 (PDT)
From: Doug Skrecky <>
Subject: Fish Oil Holds Promise In Alzheimer's Fight

[Suggested taste test: Try salmon versus hamburger.]

Fish Oil Holds Promise In Alzheimer's Fight
WASHINGTON -- Even our grandmothers told us fish was "brain
food"--and now scientists have evidence to back the claim.

Researchers with the Department of Veterans Affairs (VA) and
the University of California at Los Angeles (UCLA) found that
a diet high in docosahexenoic acid, or DHA--an omega-3 fatty
acid found in relatively high concentrations in cold-water
fish--dramatically slowed the progression of Alzheimer's
disease in mice. Specifically, DHA cut the harmful brain
plaques that mark the disease. The results appear in the
March 23 online edition of the Journal of Neuroscience.

Senior author Greg M. Cole, Ph.D., a neuroscientist at the
Greater Los Angeles VA Healthcare System and UCLA, said that
unlike many studies with mice, this one points to the benefits
of a therapy that is easily available and already touted for
other medical conditions. DHA--either from food sources such as
fish and soy, or in fish-oil supplements--is recommended by many
cardiologists for heart health, based on scores of previous
studies.

"The good news from this study is that we can buy the therapy
at a supermarket or drug store," said Cole. "DHA has a
tremendous safety profile--essentially no side effects--and
clinical trial evidence supports giving DHA supplements to
people at risk for cardiovascular disease."

The new study involved older mice genetically altered to develop
Alzheimer's disease. The researchers fed one group of the mice
DHA-fortified chow. The control mice ate a normal or DHA-depleted
diet.

After three to five months--the equivalent of several years in
human biology--the high-DHA group had 70-percent less buildup
of amyloid protein in the brain. This sticky protein makes up
the plaques, or patches, that are a hallmark of Alzheimer's.

A similar study by Cole's group published in Neuron last fall
showed that DHA protected against damage to the "synaptic" areas
where brain cells communicate and enabled mice to perform better
on memory tests.

The studies, say the scientists, suggest that even people who
are genetically predisposed to the disease may be able to delay
it by boosting their DHA intake.

Omega-3 fatty acids, typically deficient in the American diet,
are essential for human health. DHA in particular is vital to
proper brain function, as well as eye health and other body
processes. In recent years epidemiologists have tied fish-rich
diets to a lower incidence of Alzheimer's disease and homed in
on DHA as the preventive factor. Omega-3 fatty acid supplements
are now being tested in clinical trials with early-stage
Alzheimer's patients in the United States, Canada and Sweden to
see if the therapy really slows the disease.

Food sources of omega-3 fatty acids include fish such as salmon,
halibut, mackerel and sardines, as well as almonds, walnuts, soy,
and DHA-enriched eggs. Concerns about mercury contamination in
fish have helped popularize purified DHA supplements based on
fish oil or algae. Last year, Cole's team identified another
nutrient that appears to combat Alzheimer's plaques in mice:
curcumin, the yellow pigment in turmeric, one of the spices that
make up curry powder. Researchers became interested in curcumin's
potential to prevent or treat Alzheimer's disease after noting the
low prevalence of dementia among the elderly in India, where curry
is a staple.

J Neurosci. 2005 Mar 23;25(12):3032-40.
A diet enriched with the omega-3 fatty acid docosahexaenoic acid
reduces amyloid burden in an aged Alzheimer mouse model.
Epidemiological studies suggest that increased intake of the
omega-3 (n-3) polyunsaturated fatty acid (PUFA) docosahexaenoic
acid (DHA) is associated with reduced risk of Alzheimer's disease
(AD). DHA levels are lower in serum and brains of AD patients,
which could result from low dietary intake and/or PUFA oxidation.
Because effects of DHA on Alzheimer pathogenesis, particularly on
amyloidosis, are unknown, we used the APPsw (Tg2576) transgenic
mouse model to evaluate the impact of dietary DHA on amyloid
precursor protein (APP) processing and amyloid burden. Aged animals
(17-19 months old) were placed in one of three groups until 22.5
months of age: control (0.09% DHA), low-DHA (0%), or high-DHA (0.6%)
chow. beta-Amyloid (Abeta) ELISA of the detergent-insoluble extract
of cortical homogenates showed that DHA-enriched diets significantly
reduced total Abeta by >70% when compared with low-DHA or control
chow diets. Dietary DHA also decreased Abeta42 levels below those
seen with control chow. Image analysis of brain sections with an
antibody against Abeta (amino acids 1-13) revealed that overall
plaque burden was significantly reduced by 40.3%, with the largest
reductions (40-50%) in the hippocampus and parietal cortex. DHA
modulated APP processing by decreasing both alpha- and beta-APP
C-terminal fragment products and full-length APP. BACE1
(beta-secretase activity of the beta-site APP-cleaving enzyme),
ApoE (apolipoprotein E), and transthyretin gene expression were
unchanged with the high-DHA diet. Together, these results suggest
that dietary DHA could be protective against beta-amyloid
production, accumulation, and potential downstream toxicity.

[Note: Go easy on mackerel. This fish tends to accumulate mercury, while
salmon does not.]

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