Affiliation:
1. School of Biomedical Sciences, Kent State University, Ohio, United States
Abstract
Type II Diabetes (T2D) is a major risk factor for Alzheimer’s Disease (AD). These two diseases share
several pathological features, including amyloid accumulation, inflammation, oxidative stress, cell death and
cognitive decline. The metabolic hormone amylin and amyloid-beta are both amyloids known to self-aggregate in
T2D and AD, respectively, and are thought to be the main pathogenic entities in their respective diseases. Furthermore,
studies suggest amylin’s ability to seed amyloid-beta aggregation, the activation of common signaling
cascades in the pancreas and the brain, and the ability of amyloid beta to signal through amylin receptors
(AMYR), at least in vitro. However, paradoxically, non-aggregating forms of amylin such as pramlintide are given
to treat T2D and functional and neuroprotective benefits of amylin and pramlintide administration have been
reported in AD transgenic mice. These paradoxical results beget a deeper study of the complex nature of amylin’s
signaling through the several AMYR subtypes and other receptors associated with amylin effects to be able to
fully understand its potential role in mediating AD development and/or prevention. The goal of this review is to
provide such critical insight to begin to elucidate how the complex nature of this hormone’s signaling may explain
its equally complex relationship with T2D and mechanisms of AD pathogenesis.
Funder
National Institute on Aging
Publisher
Bentham Science Publishers Ltd.
Subject
Drug Discovery,Pharmacology
Cited by
4 articles.
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