Florin Despa, PhD, University of Kentucky, Lexington, KY, shares his thoughts on the therapeutic potential of pancreatic amylin clearance in Alzheimer’s disease (AD). Research from the Despa lab has demonstrated that hyperamylinemia can lead to systemic inflammation and co-deposition of amylin and amyloid β (Aβ) in the cerebral microvasculature, consequently blocking the transport of Aβ out of the brain. It has therefore been hypothesized that lowering pancreatic amylin levels may improve the clearance of Aβ from brains with AD pathology. Dr Despa highlights the challenges associated with suppressing amylin secretion given that beta cells co-secrete amylin alongside insulin. To avoid metabolic dyshomeostasis, an anti-amylin therapy would need to reduce amylin levels without impacting glucose secretion. Acting on secreted amylin rather than beta cells may be one way to achieve this. This interview took place at the Clinical Trials on Alzheimer’s Disease congress 2022 in San Francisco.
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