What is it about?
Clearance of aberrant protein fragments is essential for neuronal health, and this process is disrupted in Alzheimer's disease (AD). We demonstrate how excess intracellular Ca2+, an early feature of AD , drives this pathogenic process in human neurons.
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Why is it important?
We identified a key pathogenic mechanism which links seemingly disparate components of AD, and show how excess calcium release through a specific channel interferes with critical protein handling processes and drives accumulation of protein aggregates diagnostic of AD. Importantly, by treating human AD neurons with a calcium channel inhibitor, normal neuronal functions and protein levels are restored. Thus these findings provide a novel therapeutic approach that addresses mechanisms associated with memory loss as well pathological protein aggregations.
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This page is a summary of: Protein mishandling and impaired lysosomal proteolysis generated through calcium dysregulation in Alzheimer’s disease, Proceedings of the National Academy of Sciences, November 2022, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.2211999119.
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