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CTAD 2022 | Systemic inflammation and reduced cerebral Aβ clearance triggered by pancreatic amylin

Florin Despa, PhD, University of Kentucky, Lexington, KY, gives an insight into the current interest in the potential association between the pathological processes in type-2 diabetes and Alzheimer’s disease (AD). Amylin, which is a blood glucose regulating hormone together with insulin, crosses the blood-brain barrier and interacts with beta amyloid (Aβ) to form mixed amylin-Aβ deposits in the brain and cerebral vasculature. It is thought that hypersecretion of pancreatic amylin may influence Alzheimer’s pathogenesis by altering Aβ clearance. To investigate this hypothesis, researchers assessed blood amylin concentrations and their association with brain parenchymal and vascular Aβ levels. Blood and brain tissue samples from over 170 individuals were collected. Blood amylin concentrations and levels of CD14+ monocytes positive for amylin, reflecting systemic inflammation, were shown to be higher in those with dementia compared to cognitively unimpaired individuals. Brain amylin concentrations were also higher in the dementia cohort, compared to controls, and levels were associated with Aβ42 concentrations. Immunohistochemistry analyses indicated co-localization of amylin and Aβ in blood vessel walls and perivascular spaces. Overall, these findings indicate that hyperamylinemia and resultant amylin accumulation in circulating monocytes leads to increased cerebrovascular amylin deposition, disturbing Aβ clearance through interstitial fluid drainage along vascular walls. This interview took place at the Clinical Trials on Alzheimer’s Disease congress 2022 in San Francisco.

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