Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1863, Issue 5, Pages 1078-1089Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2016.08.018
Keywords
Alzheimer's disease; Obesity; BMI; diabetes; Type-3-Diabetes; MCI amyloid beta; Tau; GSK3 beta
Funding
- NIH [AG042178, AG047812]
- Garrison Family Foundation
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Recently researchers proposed the term 'Type-3-Diabetes' for Alzheimer's disease (ad) because of the shared molecular and cellular features among Type-1-Diabetes, Type-2-Diabetes and insulin resistance associated with memory deficits and cognitive decline in elderly individuals. Recent clinical and basic studies on patients with diabetes and AD revealed previously unreported cellular and pathological among diabetes, insulin resistance and AD. These studies are also strengthened by various basic biological studies that decipher the effects of insulin in the pathology of AD through cellular and molecular mechanisms. For instance, insulin is involved in the activation of glycogen synthase kinase 313, which in turn causes phosphorylation of tau, which involved in the formation of neurofibrillary tangles. Interestingly, insulin also plays a crucial role in the formation amyloid plaques. In this review, we discussed significant shared mechanisms between AD and diabetes and we also provided therapeutic avenues for diabetes and AD. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondria) Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases-edited by P. Hemachandra Reddy. (C) 2016 Elsevier B.V. All rights reserved.
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