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Another Group Argues for Alzheimer's Disease to be a Diabetic Condition


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Posted 01 December 2016 - 02:17 PM


A number of the aspects of Alzheimer's disease biochemistry have a strong similarity to aspects of type 2 diabetes biochemistry. Alzheimer's also has the same risk factors, such as the presence of excess visceral fat tissue. Some researchers have gone so far as to call for the classification of Alzheimer's as type 3 diabetes. While not official, there has been enough of this sort of discussion over the years that when type 4 diabetes was discovered it had to be called type 4 in order to avoid the inevitable confusion. It is very unclear as to where the diabetic aspects of Alzheimer's disease fit in the long chain of cause and effect that leads from fundamental damage that causes aging to age-related disease, and so equally unclear as to how effective it can be in the best case to undertake efforts to adjust this biochemistry. Nonetheless, the research linked here is one of many examples in which Alzheimer's has facets that strongly resemble diabetes:

Researchers have found a promising treatment for Alzheimer's disease, by noticing a similarity in the way insulin signaling works in the brain and in the pancreas of diabetic patients. In the pancreas, the Kir6.2 channel blockade increases the insulin signaling, and insulin signaling decreases the blood glucose levels. In the brain, insulin signaling increases the acquisition of memory through CaM kinase II activation by Kir6.2 channel blockade. The research group thus concluded that Alzheimer's disease can be described as a diabetic disorder of the brain. Memantine, a drug widely used to treat Alzheimer's disease, is a well known inhibitor of the N-methyl-D-aspartate (NMDA) receptors that prevent excessive glutamate transmission in the brain. Researchers have now found that memantine also inhibits the ATP-sensitive potassium channel (Kir6.2 channel), improving insulin signal dysfunction in the brain.

In their experiment with mice, the researchers found that memantine treatment improved impaired hippocampal long-term potentiation (LTP) and memory-related behaviors in the mice through the inhibition of KATP channel Kir6.2. "Our results suggest that Kir6.2 blockade in dendritic spines by memantine regulates CaMKII activity by increasing intracellular Ca2+ mobilization, which in turn improves cognitive function by promoting AMPAR trafficking into the postsynaptic membrane. Since KATP channels Kir6.1 or Kir6.2 are critical components of sulfonylurea receptors (SURs) which is downstream insulin receptor signaling, the KATP channel inhibition by Memantine mediates the anti-diabetic drug action in peripheral tissues. And this leads to improved cognitive functions and improved memory retention among Alzheimer's patients." The researchers now hope that results of their study and the parallels drawn with diabetes, will lead to new treatments for Alzheimer's disease, using the inhibition of Kir6.2 channel.

Link: http://www.tohoku.ac...n_disorder.html


View the full article at FightAging




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