Title:Bloodborne Pancreatic Amylin, a Therapeutic Target for Alzheimer's
Disease
Volume: 19
Issue: 14
Author(s): Florin Despa*
Affiliation:
- Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY, USA
Keywords:
Brain accumulation amyloid β (Aβ), Alzheimer disease (AD), Bloodborne pancreatic amylin, neurofibrillary tau tangles, neurodegeneration, bloodborne.
Abstract: Alzheimer Disease (AD) pathology has been linked to brain accumulation of β amyloid
(Aβ) and neurofibrillary tau tangles. An intriguing question is whether targeting factors independent of
Aβ and tau pathologies could delay or even stop neurodegeneration. Amylin, a pancreatic hormone cosecreted
with insulin, is believed to play a role in the central regulation of satiation and was shown to
form pancreatic amyloid in persons with type-2 diabetes mellitus. Accumulating evidence demonstrates
that amyloid-forming amylin secreted from the pancreas synergistically aggregates with vascular
and parenchymal Aβ in the brain in both sporadic and early-onset familial AD. Pancreatic expression
of amyloid-forming human amylin in AD-model rats accelerates AD-like pathology, whereas genetically
suppressed amylin secretion protects against AD effects. Thus, current data suggest a role of
pancreatic amyloid-forming amylin in modifying AD; further research is required to test whether lowering
circulating amylin levels early during AD pathogenesis may curb cognitive decline.
