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Abstract
The calcium ion (Ca2+) plays fundamental roles in orchestrating dynamic changes in the function and structure of nerve cell circuits in the brain. The endoplasmic reticulum (ER), an organelle that actively removes Ca2+ from the cytoplasm, can release stored Ca2+ through ER membrane receptor channels responsive either to the lipid messenger inositol trisphosphate(IP3) or to cytosolic Ca2+. Emerging findings suggest that perturbed ER Ca2+ homeostasis contributes to the dysfunction and degeneration of neurons that occurs in Alzheimer’s disease (AD). Presenilin-1 (PS1) is an integral membrane protein in the ER; mutations in PS1 that cause early-onset inherited AD increase the pool of ER Ca2+ available for release and also enhance Ca2+ release through ER IP3- and ryanodine-sensitive channels. By enhancing Ca2+ flux across the ER membrane, PS1 mutations may exaggerate Ca2+ signaling in synaptic terminals and thereby render them vulnerable to dysfunction and degeneration in the settings of aging and amyloid accumulation in AD.
