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TL;DR
The review highlights physicochemical similarities between hIAPP and Alzheimer's disease (AD)-associated amyloid-beta (Aβ), including their shared degradation by enzymes like insulin-degrading enzyme.
Diabetology & Metabolic Syndrome · 7 authors, 7 centres
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The review highlights physicochemical similarities between hIAPP and Alzheimer's disease (AD)-associated amyloid-beta (Aβ), including their shared degradation by enzymes like insulin-degrading enzyme.
The review highlights physicochemical similarities between hIAPP and Alzheimer's disease (AD)-associated amyloid-beta (Aβ), including their shared degradation by enzymes like insulin-degrading enzyme. Central findings suggest hIAPP and Aβ can interact synergistically, with mixed oligomers showing enhanced neurotoxicity, particularly in hippocampal neurons. Potential shared pathogenic mechanisms in T2D and AD include oxidative stress, mitochondrial dysfunction, dysregulated autophagy, abnormal heparan sulfate proteoglycans, exaggerated immune responses, and zinc dyshomeostasis, all of which may promote hIAPP aggregation and cross-toxicity. The review suggests DPP-4 inhibitors and GLP-1 agonists may attenuate AD in T2D by reducing hIAPP, but calls for more research to clarify the link.