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Do microglia default on network maintenance in Alzheimer's disease?


Southam, KA and Vincent, AJ and Small, DH, Do microglia default on network maintenance in Alzheimer's disease?, Journal of Alzheimer's Disease, 51, (3) pp. 657-669. ISSN 1387-2877 (2016) [Refereed Article]


Copyright Statement

Copyright 2016 IOS Press and the authors. All rights reserved This article is published online with Open Access and distributed under the terms of the Creative Commons Attribution Non-Commercial License.

DOI: doi:10.3233/JAD-151075


Although the cause of Alzheimer's disease (AD) remains unknown, a number of new findings suggest that the immune system may play a critical role in the early stages of the disease. Genome-wide association studies have identified a wide array of risk-associated genes for AD, many of which are associated with abnormal functioning of immune cells. Microglia are the brain's immune cells. They play an important role in maintaining the brain's extracellular environment, including clearance of aggregated proteins such as amyloid-β (Aβ). Recent studies suggest that microglia play a more active role in the brain than initially considered. Specifically, microglia provide trophic support to neurons and also regulate synapses. Microglial regulation of neuronal activity may have important consequences for AD. In this article we review the function of microglia in AD and examine the possible relationship between microglial dysfunction and network abnormalities, which occur very early in disease pathogenesis.

Item Details

Item Type:Refereed Article
Keywords:microglia, network abnormalities, neural networks, phagocytosis, synapse pruning
Research Division:Biomedical and Clinical Sciences
Research Group:Neurosciences
Research Field:Central nervous system
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Southam, KA (Dr Katherine Southam)
UTAS Author:Vincent, AJ (Dr Adele Vincent)
UTAS Author:Small, DH (Professor David Small)
ID Code:107616
Year Published:2016
Web of Science® Times Cited:14
Deposited By:Menzies Institute for Medical Research
Deposited On:2016-03-21
Last Modified:2022-08-23
Downloads:128 View Download Statistics

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