Role Of Astrocytes In Thiamine Deficiency

dc.creatorAfadlal S.
dc.creatorLabetoulle R.
dc.creatorHazell A.S.
dc.date2014
dc.date2015-06-25T18:06:11Z
dc.date2015-11-26T15:07:00Z
dc.date2015-06-25T18:06:11Z
dc.date2015-11-26T15:07:00Z
dc.date.accessioned2018-03-28T22:17:25Z
dc.date.available2018-03-28T22:17:25Z
dc.identifier
dc.identifierMetabolic Brain Disease. Springer New York Llc, v. 29, n. 4, p. 1061 - 1068, 2014.
dc.identifier8857490
dc.identifier10.1007/s11011-014-9571-y
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84911805787&partnerID=40&md5=14ae2fbbc10660a7941fcadd939cf0b5
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/88215
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/88215
dc.identifier2-s2.0-84911805787
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1257356
dc.descriptionThiamine deficiency (TD) is the underlying cause of Wernicke’s encephalopathy (WE), an acute neurological disorder characterized by structural damage to key periventricular structures in the brain. Increasing evidence suggests these focal histological lesions may be representative of a gliopathy in which astrocyte-related changes are a major feature of the disorder. These changes include a loss of the glutamate transporters GLT-1 and GLAST concomitant with elevated interstitial glutamate levels, lowered brain pH associated with increased lactate production, decreased levels of GFAP, reduction in the levels of glutamine synthetase, swelling, alterations in levels of aquaporin-4, and disruption of the blood–brain barrier. This review focusses on how these manifestations contribute to the pathophysiology of TD and possibly WE.
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dc.languageen
dc.publisherSpringer New York LLC
dc.relationMetabolic Brain Disease
dc.rightsfechado
dc.sourceScopus
dc.titleRole Of Astrocytes In Thiamine Deficiency
dc.typeArtículos de revistas


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