title: How dependent is synaptic plasticity on microglial phenotype?
abstract: Microglia are particularly plastic cells which can be shifted from their resting state by numerous factors and adopt distinct phenotypes. The cells are multifunctional, though their main role is probably maintenance of homoeostasis. Resting cells are responsible for surveillance, whereas activation induces the cells to adopt neuroprotective or neurodetrimental roles, which are anti-inflammatory or pro-inflammatory respectively. The evidence indicates that activated cells with a pro-inflammatory phenotype predominate in neurodegenerative diseases and models of neurodegeneration and that this may significantly contribute to the deteriorating neuronal function. This question is considered in this review, in particular in the context of animal models of Alzheimer's disease (AD). This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.
authors.affiliation: Trinity College Institute of Neuroscience, Department of Physiology, Trinity College, Dublin 2, Ireland. Electronic address: jonesrs@tcd.ie.
authors.forename: Raasay S
authors.initials: RS
authors.lastname: Jones
authors.affiliation: Trinity College Institute of Neuroscience, Department of Physiology, Trinity College, Dublin 2, Ireland.
authors.forename: Marina A
authors.initials: MA
authors.lastname: Lynch
mesh_terms: D000544:Alzheimer Disease / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000502:physiology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004660:Encephalitis / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D018836:Inflammation Mediators; D017774:Long-Term Potentiation; D017628:Microglia / Q000378:metabolism / Q000502:physiology*; D010641:Phenotype
chemical_list: D016229:Amyloid beta-Peptides; D016207:Cytokines; D018836:Inflammation Mediators
keywords: Age; Alzheimer's disease; Astrocytes; Inflammatory cytokines; Microglia; Neuroinflammation; Neuronal function