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The calcium ion (Ca2+) controls neuronal network activity, synapse function and synaptic plasticity, and is a fundamental mediator of learning and memory. With aging and much more so in Alzheimer’s disease the ability of neurons to properly regulate their intracellular Ca2+ levels becomes compromised. Evidence from human and laboratory animal studies have provided compelling evidence that excessive elevation of Ca2+ levels in neurons results in their dysfunction and degeneration in Alzheimer’s disease, as well as in Parkinson’s disease, and stroke. In this episode, I talk with Professor Beth Stutzmann about her research which has advanced an understanding about how calcium regulation becomes disrupted in neurons in Alzheimer’s disease. Her findings point to excessive release of Ca2+ from intracellular pools (in the endoplasmic reticulum) as being particularly important in Alzheimer’s. This research points to new therapeutic interventions for this devastating disease. LINKS Stutzmann laboratory: https://www.rosalindfranklin.edu/acad... Relevant articles: https://pmc.ncbi.nlm.nih.gov/articles... https://pmc.ncbi.nlm.nih.gov/articles... https://pmc.ncbi.nlm.nih.gov/articles... https://pmc.ncbi.nlm.nih.gov/articles...