Bloodborne Pancreatic Amylin, a Therapeutic Target for Alzheimer's Disease

Research output: Contribution to journalArticlepeer-review

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 co-secreted 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 demon-strates 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 ge-netically 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 low-ering circulating amylin levels early during AD pathogenesis may curb cognitive decline.

Original languageEnglish
Pages (from-to)905-908
Number of pages4
JournalCurrent Alzheimer Research
Volume19
Issue number14
DOIs
StatePublished - 2022

Bibliographical note

Publisher Copyright:
© 2022 Bentham Science Publishers.

Keywords

  • Alzheimer disease (AD)
  • Bloodborne pancreatic amylin
  • Brain accumulation amyloid β (Aβ)
  • bloodborne
  • neurodegeneration
  • neurofibrillary tau tangles

ASJC Scopus subject areas

  • General Medicine

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