Should Alzheimer's Be Renamed Type III Diabetes?
> 10/22/2007 1:29:19 PM

There has been no solid consensus on the biological cause of neural degeneration in Alzheimer's patients. The majority of researchers point to the suspicious plaques that amyloid-beta forms in the brain, but suspicious presence alone is not enough to prove causation. In a breakthrough study, published in the Journal of the Federation of American Societies for Experimental Biology by Dr. Wei-Qin Zhao, the exact mechanism through which plaques impair memory is illuminated. Surprisingly, it has to do with the inability to utilize insulin, just as with Type II diabetes.

There have been suggestions in the past that Alzheimer's is a hormone problem, but only recently has research into this hypothesis grown promising. When Doctor Suzanne de la Monte discovered that the brain produces a supply of insulin independent of the rest of the body, she had an intuition that the hormone must play a crucial role in brain function. Last year, Dr. Monte published a study in the Journal of Alzheimer's Disease demonstrating that depleting insulin in the brains of rats produced neural degeneration in a pattern similar to Alzheimer's. This study did not explain how Alzheimer's interfered with insulin, but it did make a strong case for the idea that insulin deprivation is tied to brain malfunction. Later studies trying insulin in the brain to memory formation gave further support to Dr. Monte's intuition.

With the arrival of fall this year, there also came definitive evidence for the "Type III Diabetes" theory proposed by Dr. Monte—amyloid beta was observed directly corrupting insulin receptors. Dr. Wei-Qin Zhao grew a culture of hippocampal neurons in his laboratory. He found that the dendrites covered in amyloid-beta plaque did not respond appropriately to insulin because they had significantly fewer working insulin receptors.

It seems clear now that amyloid-beta interferes with insulin in the brain, and thus causes the memory impairment that is usually the first sign of Alzheimer's. However, there are many questions remaining. We still do not know whether amyloid-beta plaque causes Alzheimer's, or whether it is a symptom. If it is a symptom, then we must ask whether it is the only symptom or only one of them. It is possible that memory impairment, confusion, personality change, etc. are caused by separate mechanisms. Even if insulin interference is only one mechanism, it is imperative that we try to combat it. If treatments for normal Type II diabetes can be adapted to circumvent insulin problems in the brain, then millions of elderly sufferers may be able to hang onto their cherished memories.

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