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Old 10-20-2008, 07:51 AM   #1
Darryl Shaw
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Default Fatty acids clue to Alzheimer's.

Dr Rene Sanchez-Mejia, who worked on the study, said: "The most striking change we discovered in the Alzheimer's mice was an increase in arachidonic acid and related metabolites [products] in the hippocampus, a memory centre that is affected early and severely by Alzheimer's disease."

He suggested too much arachidonic acid might over-stimulate brain cells, and that lowering levels allowed them to function normally.

Dr Lennart Mucke, who led the research, added: "In general, fatty acid levels can be regulated by diet or drugs.

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Old 10-20-2008, 10:23 AM   #2
Garrett Smith
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Since insulin resistance creates all sorts of fatty acid regulation abnormalities, triglycerides being only one, I'd be more prone to look towards the diet first (as in blood sugar imbalancing foods, not animal proteins with their AA).

Alzheimer's Disease Could Be A Third Form Of Diabetes

"Regulating" fatty acids with drugs is a bad idea, look at the track record of statins for that one...
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Old 10-20-2008, 10:39 AM   #3
Mike ODonnell
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Bad diet/no exercise ----> Increased insulin production ----> increased inflammation ---> Increased insulin resistance of the brain ---> increased pro-inflammatory AA production ----> increased resistance ----> and on and on......

Best approach is of course diet low in direct AA ingestion (grain fed animals), low in pro-inflammatory/insulin producing foods (excess grains/sugars) and higher in Omega 3 EPA/DHA (which is EPA anti-inflammatory plus DHA improves brain function). Also need to block the internal conversion of DGLA to AA with insulin control and EPA. High insulin signals conversion to AA, EPA blocks conversion. Higher fat diet is important for people with any brain disorder to help reverse the problem. Drugs are never the best answer.....a smart diet is.

Autophagy is also an important part and related to proper brain neuro-function:

The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid β accumulation in mice

In summary, we identified beclin 1 and autophagy as important modulators of neurodegeneration and Aβ accumulation in a mouse model for AD. We also found beclin 1 was significantly reduced in early stages of AD in affected brain regions. Because overexpression of beclin 1 can reduce Aβ pathology in mice, restoring beclin 1 and autophagy may be novel approaches to treat AD.
“We discovered that levels of several key pathway members are reduced in Drosophila neural tissue as a normal part of aging,” says senior author Kim Finley, Ph.D., a scientist in the Cellular Neurobiology Laboratory, “which suggests there is an age-dependent suppression of autophagy that may be a contributing factor for human neurodegenerative disorders like Alzheimer’s disease.”

“The activation of autophagy facilitates the removal of damaged molecules that accumulate during cellular aging,” says Finley. “This may be particularly important in the nervous system since neurons produce damaged molecules at a much higher rate than most cell types.” Keeping cells free of damaged molecules is critical for neurons because unlike many cells, they do not divide or replace themselves once created at birth. “They rely on autophagy together with other clearance and detoxification pathways to keep themselves healthy and functioning for decades,” explains Finley.

Insulin signaling and caloric restriction are two major determinants of longevity and they also impact the activity level of autophagy. Therefore, regulating autophagy, the pathway that directly does the cleanup work, may be the key factor in controlling the aging process, the researchers say. “By maintaining the expression of a rate-limiting autophagy gene in the aging nervous system there is a dramatic extension of lifespan and resistance to age-associated oxidative stress,” says Finley.
Also a great article on autophagy in Scientific American May 2008.
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Last edited by Mike ODonnell; 10-20-2008 at 11:09 AM.
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Old 10-20-2008, 11:31 AM   #4
Garrett Smith
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So I went looking for the relationship between insulin, diabetes, and arachidonic acid. I find this stuff entertaining (and educational).

Here's an interesting path to go down.

So, Darryl's original post showed that AA is elevated in Alzheimer's Disease. Cool, got it. Why is it elevated, and is the AA really the problem, is it simply a symptom of something else, or is it an effort by the body to protect brain cells? So, here's what I found:

My original link was talking about brain cells becoming insulin resistant.

Glucose-induced protein kinase C activity regulates arachidonic acid release and eicosanoid production by cultured glomerular mesangial cells.

Changes in glomerular eicosanoid production have been implicated in the development of diabetes-induced glomerular hyperfiltration and glomerular mesangial cells (GMC) are major eicosanoid-producing cells within the glomerulus. However, the mechanism for the effect of diabetes mellitus on glomerular mesangial eicosanoid production is unknown. The present study therefore examined whether elevated glucose concentrations activate protein kinase C (PKC) in GMC and whether this PKC activation mediates an effect of elevated glucose concentrations to increase the release of arachidonic acid and eicosanoid production by GMC.[...].These data demonstrate that elevated extracellular glucose concentrations directly increase the release of endogenous arachidonic acid and eicosanoids by GMC via mechanisms dependent on glucose-induced PKC activation.
Yes, the above is talking about kidney cells. It also shows that increased extracellular concentrations of glucose (as in insulin resistance and hyperglycemia) increases arachidonic acid production by those cells.

Arachidonic Acid Can Significantly Prevent Early Insulin Resistance Induced by a High-Fat Diet

Aim: To investigate whole-body metabolic disorder and hepatic glucose output (HGO) disturbance in rats with insulin resistance induced by a short-term high-fat diet, and the effect of arachidonic acid (AA).[...].Conclusion: AA can significantly prevent whole-body insulin resistance induced by a high-fat diet, as well as accompanied HGO disturbance in the overnight fasting state, but not thoroughly.
So, maybe the body is creating the AA specifically because it is trying to protect and reverse the insulin resistance in the brain cells.

Protective action of arachidonic acid against alloxan-induced cytotoxicity and diabetes mellitus

Here we show that alloxan-induced in vitro cytotoxicity and apoptosis in an insulin secreting rat insulinoma, RIN, cells can be prevented by arachidonic acid (AA) and that both cyclo-oxygenase and lipoxygenase inhibitors do not block this protective action. Alloxan-induced diabetes in male Wistar rats was also prevented by oral supplementation of AA, gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). This protective action is best when the animals were pre-treated with the fatty acid. These results suggest that polyunsaturated fatty acids can prevent alloxan-induced diabetes mellitus in experimental animals and may be useful to prevent diabetes mellitus in the high-risk population.
Apparently, the body's attempt to produce AA may be a case of too little, too late (as pretreatment with the fatty acids was the best, ounce of prevention, pound of cure and all...). Again, AA is found to be protective.

It would seem the AA & Alzheimer's study was another one trying to go into the "lipid hypothesis", and yet again, all of it can be brought back to insulin resistance.
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