September 28, 2007
Alzheimers Protein Causes Insulin Resistant Diabetes In Brain

Here is more evidence htat Alzheimer's Diseases is a type of insulin resistant diabetes.

EVANSTON, Ill. --- Insulin, it turns out, may be as important for the mind as it is for the body. Research in the last few years has raised the possibility that Alzheimer’s memory loss could be due to a novel third form of diabetes.

Now scientists at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer’s disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer’s removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for “amyloid ß-derived diffusible ligand.”)

With other research showing that levels of brain insulin and its related receptors are lower in individuals with Alzheimer’s disease, the Northwestern study sheds light on the emerging idea of Alzheimer’s being a “type 3” diabetes.

Insulin serves multiple functions. The best known is that it binds on the surface of cells and causes the cells to pull sugar out of the bloodstream. But the lack of binding by insulin on neurons in Alzheimer's might wreak damage due to interference with other processes which insulin helps regulate.

Development of the ability to block the accumulation of these ADDL proteins might provide a way to stop Alzheimer's. But the research on insulin resistance in Alzheimer's suggests that treatments used for type 2 insulin resistant diabetes might help also. Or drugs could be developed to block ADDL binding to insulin receptors.

“We found the binding of ADDLs to synapses somehow prevents insulin receptors from accumulating at the synapses where they are needed,” said William L. Klein, professor of neurobiology and physiology in the Weinberg College of Arts and Sciences, who led the research team. “Instead, they are piling up where they are made, in the cell body, near the nucleus. Insulin cannot reach receptors there. This finding is the first molecular evidence as to why nerve cells should become insulin resistant in Alzheimer’s disease.”

ADDLs are small, soluble aggregated proteins. The clinical data strongly support a theory in which ADDLs accumulate at the beginning of Alzheimer’s disease and block memory function by a process predicted to be reversible.

Alzheimer's is a horrible disease. Your brain slowly dies while your body remains living. You know it is happening until you reach the point where you can't even remember that much.

Why do the ADDLs accumulate in the first place? We need treatments that will stop Alzheimer's by stopping the very earliest steps in the disease. Is toxic protein accumulation the earliest step? Or is the earliest step something that causes the toxic proteins to start accumulating?

Share |      Randall Parker, 2007 September 28 08:40 AM  Brain Alzheimers Disease


Comments
Sam said at September 28, 2007 5:39 PM:

If treatments for Type II diabetes would work, wouldn't that have showed up in epidemiological data? Like an increased risk for Alzheimer's in people with diabetes or metabolic syndrome. Is there any such correlation, or is this a totally different role for insulin?

Randall Parker said at September 28, 2007 8:12 PM:

Sam,

My guess is that insulin is binding on a different receptor in neurons and probably even for a different effect.

BTW, insulin does lots of things other than regulate passage of sugar into cells.

Rob said at September 30, 2007 10:09 AM:

Randall,

At least one study has shown that a ketogenic diet reduces the plaques in alzheimer mice. http://www.sciencedaily.com/releases/2005/10/051017072307.htm

It does not seem unreasonable that people evolved to be hungry at least occassionally, and since fasting is unpleasant, going into ketosis occasionally might be a good idea.

Post a comment
Comments:
Name (not anon or anonymous):
Email Address:
URL:
Remember info?

                       
Go Read More Posts On FuturePundit
Site Traffic Info
The contents of this site are copyright ©