Affiliations: [a] School of Biomedical Sciences, Kent State University, Kent, OH, USA
| [b] Department of Biological Sciences, Kent State University, Kent, OH, USA
Correspondence:
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Correspondence to: Gemma Casadesus, PhD, 256 Cunningham Hall, Department of Biological Sciences, Kent State University, Kent, Ohio 44242, USA. Tel.: +1 330 672 7894; Fax: +1 330 672 3713; E-mail: gcasades@kent.edu.
Abstract: Type II diabetes (T2D) has been identified as a major risk factor for the development of Alzheimer’s disease (AD). Interestingly, both AD and T2D have similar characteristics including amyloid peptide aggregation, decreased metabolism, and increased oxidative stress and inflammation. Despite their prevalence, therapies for these diseases are limited. To date, most therapies for AD have targeted amyloid-β or tau. Unfortunately, most of these clinical trials have been largely unsuccessful, creating a crucial need for novel therapies. A number of studies have shown that metabolic hormone therapies are effective at ameliorating high blood glucose levels in diabetics as well as improving cognitive function in AD and mild cognitive impairment patients. Pramlintide, a synthetic analogue of the pancreatic hormone amylin, has been developed and used for years now as a treatment for both type I diabetes and T2D due to the loss of β-islet cells responsible for producing amylin. Importantly, recent data demonstrates its potential therapeutic role for AD as well. This review aims at addressing parallels between T2D and AD at a pathological and functional level, focusing on amylin signaling as a key, overlapping mediator in both diseases. The potential therapeutic use of this hormone to treat AD will also be explored from a mechanistic viewpoint.
Keywords: Alzheimer’s disease, amylin, cognition, pramlintide, type II diabetes
