Astrocytic and microglial nicotinic acetylcholine receptors: an overlooked issue in Alzheimer's disease
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Abstract
It is increasingly recognized that astrocytes and microglia-associated dysfunction contribute to AD pathology. In addition, glial nicotinic acetylcholine receptors (nAChRs) play a role in AD-related phenomena, such as neuron survival, synaptic plasticity, and memory. From mechanistic point of view, the glial regulation of pro-inflammatory cytokines, as common contributors in AD, is modulated by nAChRs. Astrocytic and microglial nAChRs contribute to A? metabolism, including A? phagocytosis and degradation as well as A?-related oxidative stress and neurotoxicity. These receptors are also involved in neurotransmission and gliotransmission through indirect interaction with N-Methyl-d-aspartate (NMDA) and a-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid (AMPA) receptors as well as gamma-aminobutyric acid (GABA) and intracellular calcium regulation. In addition, glial nAChRs participate in trophic factors-induced neuroprotection. This review gathers the most recent advances along with the previous data on astrocytic and microglial nAChRs role in AD pathogenesis. أ¯?آ½ 2016, Springer-Verlag Wien.
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4 aminobutyric acid, AMPA receptor, amyloid beta protein, n methyl dextro aspartic acid, nicotinic receptor, nicotinic receptor, Alzheimer disease, astrocyte, calcium cell level, human, microglia, nervous system inflammation, neuroprotection, neurotoxicity, neurotransmission, nonhuman, oxidative stress, pathogenesis, priority journal, protein function, protein metabolism, Review, Alzheimer disease, animal, metabolism, pathology, physiology, Alzheimer Disease, Animals, Astrocytes, Humans, Microglia, Receptors, Nicotinic