Another common link that is extremely nascent in its research is the common link of Insulin Degrading Enzyme (IDE) in both AD and Type 2 Diabetes. Some research has shown that the dysfunction of IDE in some shape is present in both Type 2 Diabetes and AD.
I think this proves interesting because it connects two conditions that on the surface may not have ever seemed connected. To me, it reaffirms the fact that when we look at solving any conditions/disease within the body that we need to ensure we have take a holistic approach, particularly when inflammation is a common component.
A reference for the first study, titled "Elevated butyrylcholinesterase and acetylcholinesterase may predict the development of type 2 diabetes mellitus and Alzheimer’s disease" by Allam A. Rao, Gumpeny R. Sridhar and Undurti N. Das, is: http://www.sciencedirect.com.ezproxy1.library.arizona.edu/science?_ob=MImg&_imagekey=B6WN2-4NWW6SJ-2-1&_cdi=6950&_user=56761&_orig=search&_coverDate=12%2F31%2F2007&_sk=999309993&view=c&wchp=dGLzVzz-zSkWA&md5=047efd6e6ff36de91df59d9f0f740212&ie=/sdarticle.pdf
It is interesting to consider the possibility of various similarities in the possible causes of two seemingly different pathologies, those being Alzheimer’s disease and type 2 diabetes. It has already been proven that an inflammatory response plays a pivotal role in the progression of said diseases, but the idea that the two pathways may indeed be similar might lead to a new approach on possible treatments. It has already been shown that insulin-sensitizing drugs such as thiazolidinediones can be quite effective in targeting PPARγ receptors, which result in the differentiation of new adipocytes in the subcutaneous fat tissue. Although it has been recorded that the use of such treatments may lead to an increase in body weight, the redistribution of fat out of the muscle, liver, and pancreatic beta cells results in increased insulin sensitivity. I wonder if the idea of using thiazolidinediones in concert with an anti-inflammatory treatment would prove effective in better controlling the deleterious effects of type 2 diabetes. One such treatment might include an anti-inflammatory agent which targeted butyrylcholinesterase and acetylcholinesterase.
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