Alzheimer's Disease and Omega-3 Fatty Acids
September 15, 2004
Subject: Recent research suggests that a
diet high in omega-3 fats from fish or nuts is protective against Alzheimer
A study came out in last week's issue of Neuron suggesting that omega-3
fats prevent memory loss in mice. This is consistent
with prior research which suggested that fish oil supplements might reduce
the risk of Alzheimer's in people. Other work has shown that the
fatty acid docosahexaenoic acid (DHA) is essential to brain function and
that Alzheimer's patients have lower than normal concentrations of it
in their blood.
The early memory and learning problems that mark this disease occur because
damaged brain cells fail to transmit messages consistently to each other
across the junctions between cells called synapses.
In the current study scientists at UCLA used old mice that were genetically
engineered to develop waxy protein plaques in their brains, such as those
seen in Alzheimer's. After feeding an experimental group of mice
DHA enriched food for five mice while depleting a second group, the researchers
performed an interesting experiment to test memory. They trained
the 21 month old mice to swim in a tank of warm water and climb up onto
a platform. Once the mice knew their way to the platform they raised
the water level enough to submerge the platform. They then measured
how long it took for the mice to find their way to the platform which
they now could no longer see. The DHA fed mice could find the platform
in 20 to 30 seconds while those who were DHA depleted took 50 seconds
or more to find their way.
This is called spatial memory and is the kind of memory loss which is
associated with Alzheimer's.
Our regular readers will recall a recent newsletter on niacin, statin
drugs and Alzheimer's [click to read].
Both of these medications which are typically used to lower cholesterol
and protect the heart have recently been shown to also be protective against
Alzheimer's. A similar situation exists with these Omega-3 fatty acids.
As we add them to the list of possible protective foods and supplements
for Alzheimer's, we must point out that the biggest use of these fats
is in preventing heart disease. The best sources of Omega-3 fats
of course are fish and nuts, staples of the Mediterranean diet, and unquestionably
good for the heart.
Given these various similarities in action, I am prompted to come to the
unscientific opinion that things which are good for the heart may also
be good for the brain.
We use the expression 'heart and mind' without thinking. Could it
be that these two seemingly separate systems interact more closely and
depend on similar factors in order to maintain their integrity?
A year or so back we wrote about the study on Co enzyme-Q-10 and its role
in treating Parkinson's, knowing full well that Co Q was a "heart supplement."
Now we have these examples of niacin, nuts and fish, all heart nutrients,
as brain protective.
We spend most of our time looking at health and illness through a Western
medical model which tends to view different organ systems as separate
entities. A truer model may be to view the body as an ecological
system or perhaps as a pattern of interactions more parallel to weather
or climate. Food for thought.
Neuron. 2004 Sep 2;43(5):633-45.
Docosahexaenoic Acid protects from dendritic pathology in an Alzheimer's
disease mouse model.
Calon F, Lim GP, Yang F, Morihara T, Teter B, Ubeda O, Rostaing P, Triller
A, Salem N Jr, Ashe KH, Frautschy SA, Cole GM.
Department of Medicine, University of California, Los Angeles, Los Angeles,
CA 90095 USA.
Learning and memory depend on dendritic spine actin assembly and docosahexaenoic
acid (DHA), an essential n-3 (omega-3) polyunsaturated fatty acid (PFA).
High DHA consumption is associated with reduced Alzheimer's disease (AD)
risk, yet mechanisms and therapeutic potential remain elusive. Here, we
report that reduction of dietary n-3 PFA in an AD mouse model resulted
in 80%-90% losses of the p85alpha subunit of phosphatidylinositol 3-kinase
and the postsynaptic actin-regulating protein drebrin, as in AD brain.
The loss of postsynaptic proteins was associated with increased oxidation,
without concomitant neuron or presynaptic protein loss. N-3 PFA depletion
increased caspase-cleaved actin, which was localized in dendrites ultrastructurally.
Treatment of n-3 PFA-restricted mice with DHA protected against these
effects and behavioral deficits and increased antiapoptotic BAD phosphorylation.
Since n-3 PFAs are essential for p85-mediated CNS insulin signaling and
postsynaptic proteins, these findings have implications for neurodegenerative
diseases where synaptic loss is critical, especially AD.
PMID: 15339646 [PubMed - in process]
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