Synaptic plasticity refers to the ability of neurons to strengthen or weaken synaptic efficacy in response to activity and is the basis for\nlearning and memory. Glial cells communicate with neurons and in this way contribute in part to plasticity in the CNS and to the\npathology of Alzheimer�s disease (AD), a neurodegenerative disease in which impaired synaptic plasticity is causally implicated.\nThe transient receptor potential melastatin member 2 (TRPM2) channel is a nonselective Ca2+-permeable channel expressed in\nboth glial cells (microglia and astrocytes) and neurons. Recent studies indicated that TRPM2 regulates synaptic plasticity as well as\nthe activation of glial cells. TRPM2 also modulates oxidative stress and inflammation through interaction with glial cells. As both\noxidative stress and inflammation have been implicated in AD pathology, this suggests a possible contribution of TRPM2 to disease\nprocesses. Through modulating the homeostasis of glutathione, TRPM2 is involved in the process of aging which is a risk factor\nof AD. These results potentially point TRPM2 channel to be involved in AD through glial cells. This review summarizes recent\nadvances in studying the contribution of TRPM2 in health and in AD pathology, with a focus on contributions via glia cells.
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