Study finds DHA important for Alzheimer’s patients
In the September 2 2004 issue of the journal Neuron, (http://www.neuron.org) UCLA Professor of Neurology Greg Cole, PhD, and colleagues have shown how docosahexaenoic acid (DHA), an omega-3 fatty acid found in fish oils, protects against some of the damage caused by Alzheimer’s disease (AD), in a mouse model. Epidemiologic studies have indicated an inverse association between increased intake of omega-3 fatty acids and Alzheimer’s disease risk, but whether this is a cause or an effect of the disease has been a matter of speculation.

For the current study, the UCLA team used mice bred to have the human version of a mutant amyloid precursor protein which produces the brain plaques characteristic of Alzheimer’s disease. Older animals who were already showing evidence of the Alzheimer’s lesions were fed omega-3 fatty acid depleted diets while another group of the same age was given the diet supplemented with DHA derived from algae. Two additional groups of mice who did not have the Alzheimer’s gene were provided with regimens identical to those of the treatment groups.

When the animals were examined after five months, the researchers found significant damage to the synapses of the nerve cells in the brains of the mice with Alzheimer’s disease who were on DHA deficient diet. (Synapses are the connections between nerve cells through which the cells communicate.) The changes were similar to those observed in the brains of human Alzheimer's disease patients. Supplementation with DHA helped prevent this damage, as well as providing protection against oxidative stress in the mice who received it.

In studies in which behavior was examined, the mutant mice who received low-DHA diets showed deficits in memory and learning that did not occur in mice supplemented with DHA.

The authors explained their findings by noting that oxidative stress is the probable cause of the loss of DHA, which can be controlled by increased intake of the fatty acid and should be reduced by dietary or supplementary antioxidants.

Dr Cole commented, "This is the first proof that our diets affect how our brain cells communicate with each other under the duress of Alzheimer's disease. We saw that a diet rich in DHA, or docosahexaenoic acid, dramatically reduces the impact of the Alzheimer's gene. Consuming more DHA is something the average person can easily control. Anyone can buy DHA in its purified form, fish-oil capsules, high-fat fish or DHA-supplemented eggs."

Dr Cole and colleagues conclude that the results of their research, “support the idea that increased DHA intake should be considered as a potential neuroprotective strategy for AD." (Calon F, L GP, Yang F et al, “Docosahexaenoic acid protects from dendritic pathology in an Alzheimer’s disease mouse model,” Neuron, vol 43, 633-645.)

Alzheimer’s disease
The most characteristic features of Alzheimer's disease are senile plaques of beta-amyloid peptide, neurofibrillary tangles involving tau protein, loss of synapses, and (ultimately) the death of neurons. Although neurofibrillary tangles are more closely associated with neuronal death than beta-amyloid, the evidence is becoming convincing that beta-amyloid is the factor most responsible for starting the degenerative processes of Alzheimer's disease.

Free-radical damage (oxidative stress) is a significant cause of biological aging. It is well-known that neurons are extremely sensitive to attacks by destructive free radicals. The following evidence supports the hypothesis of free-radical damage being a central cause in Alzheimer's disease (Christen 2000):

• The brain lesions present in the brains of Alzheimer's disease patients are typically associated with attacks by free radicals (for example, damage to DNA, protein oxidation, lipid peroxidation, and advanced glycosylation end products).
• Metals (such as iron, copper, zinc, and aluminum) are often present. These metals have a catalytic activity which produces free radicals.
• Beta-amyloid is aggregated and produces more free radicals in the presence of free radicals.
• Beta-amyloid toxicity is eliminated by free radical scavengers.
• Apolipoprotein E (ApoE) is subject to attacks by free radicals, and apolipoprotein E peroxidation has been correlated with Alzheimer's disease. In contrast, apolipoprotein E can act as a free radical scavenger.
• Alzheimer's disease has been linked to mitochondrial anomalies affecting cytochrome c oxidase. These anomalies may contribute to the abnormal production of free radicals.
• Free radical scavengers (such as vitamin E, selegeline, and ginkgo biloba extract) have produced promising results in Alzheimer's disease.

https://www.lifeextension.com/protocols/neurological/alzheimers-disease

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September 2004 Life Extension magazine now online!

Reports
	Cover story: Novel fiber limits sugar absorption
	Magnesium in hypertension prevention and control, by Jay S Cohen, MD
	Thyroid deficiency: Preventing a metabolic meltdown, by Raphael Kellman, MD
	An innovative new treatment for migraine, by Dr Sergey A Dzugan
Departments
	As we see it
	In the news: Omega-3 fatty acids stabilize atherosclerotic plaques; Anti-prostate cancer vaccine shows promise; Short-term statin use depletes coQ10 levels; Sex hormones implicated in prostate enlargement; Antioxidants may protect against hearing loss; Fossils record dramatic gain in human longevity; Scientists identify gene thought to control aging
	Profile: Scott Radow by Dave Tuttle
	Case History: Hormone therapy and supplements bolster weight loss efforts, by By William Davis, MD, FACC
	Ask the doctor: Nutrients for treating obsessive-compulsive disorder, by Eric V Braverman, MD
	All about supplements: I3C may reverse autoimmunity and extend lifespan, by Terri Mitchell
	September 2004 abstracts

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Dayna Dye
Editor, Life Extension Update
ddye@lifeextension.com
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