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 language | English |
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Pages (from-to) | 905-908 |
Number of pages | 4 |
Journal | Current Alzheimer Research |
Volume | 19 |
Issue number | 14 |
DOIs | |
State | Published - 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