Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 26, Issue 12, Pages 1345-1355Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612826666200318151146
Keywords
Alzheimer's disease (AD); type II diabetes (T2D); amyloid; amyloid beta; amylin; calcitonin receptor; receptor activity modifying protein (RAMP)
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Funding
- National Institutes of Aging [1R15AG050292-01A1]
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Type II Diabetes (T2D) is a major risk factor for Alzheimers 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 amylins 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 amylins 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 hormones signaling may explain its equally complex relationship with T2D and mechanisms of AD pathogenesis.
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