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Microglia and alcohol meet at the crossroads: Microglia as critical modulators of alcohol neurotoxicity

Title
Microglia and alcohol meet at the crossroads: Microglia as critical modulators of alcohol neurotoxicity
Type
Another Publication in an International Scientific Journal
Year
2018
Authors
Henriques, JF
(Author)
Other
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Portugal, CC
(Author)
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Canedo, T
(Author)
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Relvas, JB
(Author)
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Summavielle, T
(Author)
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Socodato, R
(Author)
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Journal
Title: Toxicology LettersImported from Authenticus Search for Journal Publications
Vol. 283
Pages: 21-31
ISSN: 0378-4274
Publisher: Elsevier
Other information
Authenticus ID: P-00N-8P1
Abstract (EN): Alcohol use disorders affect millions of people worldwide causing huge social and economic burden on modern society. Excessive alcohol consumption or intoxication provokes severe damage to the body inducing immune suppression, liver damage and neurological disorder. In the central nervous system (CNS), alcohol exposure can lead to neuronal loss, cognitive decline, motor dysfunction, inflammation and impairment of neuroimmune responses. Glial cells, from which microglia represent roughly 10-15%, are primary modulators of the neuroimmune responses and inflammation in the CNS. Here we overview literature relating alcohol exposure with microglia activation and brain inflammation, highlighting that microglia are critical regulators of alcohol responses in the CNS. Different studies indicate that alcohol intake alters the microglial activation spectrum, with the microglial response varying according to the dose, duration, and pattern of alcohol administration. Presently, further investigation is required to establish whether microglia dysfunction initiates or simply amplifies the neurotoxicity of alcohol in the brain. Such knowledge can be greatly facilitated by the use of microglia-specific genetic targeting in animal models and will be critical for the development of better therapeutics for mitigating the neurotoxicity induced by alcohol.
Language: English
Type (Professor's evaluation): Scientific
No. of pages: 11
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