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 's disease.


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 selective protect
 ion of
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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