| Literature DB >> 27262818 |
Saeed Sadigh-Eteghad1, Alireza Majdi2, Javad Mahmoudi1, Samad E J Golzari3, Mahnaz Talebi1.
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 Aβ metabolism, including Aβ phagocytosis and degradation as well as Aβ-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.Entities:
Keywords: Alzheimer’s disease; Astrocyte; Microglia; Nicotinic acetylcholine receptors
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Year: 2016 PMID： 27262818 DOI： 10.1007/s00702-016-1580-z
Source DB: PubMed Journal: J Neural Transm (Vienna) ISSN： 0300-9564 Impact factor: 3.575