Abstract
Type 2 diabetes (T2D) increases the risk for cerebrovascular disease (CVD) and dementia. The underlying molecular mechanisms remain elusive, which hampers the development of treatment or/and effective prevention strategies. Recent studies suggest that dyshomeostasis of amylin, a satiety hormone that forms pancreatic amyloid in patients with T2D, promotes accumulation of amylin in cerebral small blood vessels and interaction with Alzheimer's disease (AD) pathology. Overexpression of human amylin in rodents (rodent amylin does not form amyloid) leads to late-life onset T2D and neurologic deficits. In this Review, we discuss clinical evidence of amylin pathology in CVD and AD and identify critical characteristics of animal models that could help to better understand molecular mechanisms underlying the increased risk of CVD and AD in patients with prediabetes or T2D.
Document Type
Review
Publication Date
9-2019
Digital Object Identifier (DOI)
https://doi.org/10.12997/jla.2019.8.2.144
Repository Citation
Ly, Han and Despa, Florin, "Diabetes-Related Amylin Dyshomeostasis: A Contributing Factor to Cerebrovascular Pathology and Dementia" (2019). Pharmacology and Nutritional Sciences Faculty Publications. 105.
https://uknowledge.uky.edu/pharmacol_facpub/105
Notes/Citation Information
Published in Journal of Lipid and Atherosclerosis, v. 8, issue 2.
Copyright © 2019 The Korean Society of Lipid and Atherosclerosis
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.