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Presynaptic cytoplasmic Ca 2+ can be depleted by several complementary mechanisms, including sarcoendoplasmic reticulum Ca 2+ -ATPase (SERCA) to the endoplasmic reticulum (ER), plasma membrane Ca 2+ -ATPase to the extracellular space, and MCU to the mitochondrial matrix [51,52,53]

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Xu and Wang (2016) [79] used several validated algorithms to identify TMAO as a metabolite significantly associated with various aspects of Alzheimer’s disease (AD)