Hyperamylinemia as a risk factor for accelerated cognitive decline in diabetes

Han Ly, Florin Despa

Research output: Contribution to journalReview articlepeer-review

16 Scopus citations

Abstract

Type II diabetes increases the risk for cognitive decline via multiple traits. Amylin is a pancreatic hormone that has amyloidogenic and cytotoxic properties similar to the amyloid-β peptide. The amylin hormone is overexpressed in individuals with pre-diabetic insulin resistance or obesity leading to amylin oligomerization and deposition in pancreatic islets. Amylin oligomerization was implicated in the apoptosis of the insulin-producing β-cells. Recent studies showed that brain tissue from diabetic patients with cerebrovascular dementia or Alzheimers disease contains significant deposits of oligomerized amylin. It has also been reported that the brain amylin deposition reduced exploratory drive, recognition memory and vestibulomotor function in a rat model that overexpresses human amylin in the pancreas. These novel findings are reviewed here and the hypothesis that type II diabetes is linked with cognitive decline by amylin accumulation in the brain is proposed. Deciphering the impact of hyperamylinemia on the brain is critical for both etiology and treatment of dementia.

Original languageEnglish
Pages (from-to)575-577
Number of pages3
JournalExpert Review of Proteomics
Volume12
Issue number6
DOIs
StatePublished - Nov 2 2015

Bibliographical note

Publisher Copyright:
© 2015 Taylor & Francis.

Funding

The authors were supported by the Pilot Project from the University of Kentucky Alzheimer’s Disease Center: National Institute of Aging, 5P30 AG028383 Pilot Project DiaComp; the National Institute of Diabetes and digestive and Kidney Diseases, National Science Foundation CBET-1133339; National Heart, Lung, Heart and Blood Institute, R01HL118474 and the Alzheimer’s Association, VMF-15-363458. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

FundersFunder number
University of Kentucky Alzheimer’s Disease Center: National Institute of Aging5P30 AG028383
National Science Foundation (NSF)CBET-1133339
National Institutes of Health (NIH)
National Institute on AgingP30AG028383
National Heart, Lung, and Blood Institute (NHLBI)R01HL118474
National Institute of Diabetes and Digestive and Kidney Diseases
Alzheimer's AssociationVMF-15-363458

    Keywords

    • A?
    • Alzheimer's disease
    • amylin
    • amyloid
    • cerebrovascular disease
    • dementia
    • hyperamylinemia
    • hyperinsulinemia
    • insulin resistance
    • type 2 diabetes

    ASJC Scopus subject areas

    • Biochemistry
    • Molecular Biology

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