Linked Life Data

17504172

Source:http://linkedlifedata.com/resource/pubmed/id/17504172

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-5-16
pubmed:abstractText
HIV-1 infection with concurrent methamphetamine (MA) abuse results in exacerbated neurodegenerative changes and rapid progression of a form of sub-cortical dementia termed HIV-1 associated dementia (HAD). A notable feature of HAD is the involvement of the dopaminergic system manifested as parkinsonian like movement abnormalities. The HIV-1 transactivator of transcription (Tat) protein is very often used in experimental studies trying to understand neurotoxic consequences of HIV-1 infection, since the pathophysiological changes induced by Tat mirrors, in part, the means by which HIV-1 infection of the nervous system results in neuronal damage. Understanding the interaction of Tat and MA in the basal ganglia and the resultant injury to the dopaminergic system in rodent models as well as cell culture will shed light on the dopaminergic pathology occurring in HIV-1 infected-MA abusers. The aim of this review is to update the reader on the current knowledge of MA and HIV-1 neurotoxicity, specifically Tat, and discuss the progress in understanding how MA synergizes with the HIV-1 transactivator protein Tat to damage the basal ganglia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1873-4251
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
301-13
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Progress in understanding basal ganglia dysfunction as a common target for methamphetamine abuse and HIV-1 neurodegeneration.
pubmed:affiliation
Department of Neurology, The University of Alabama at Birmingham, USA. stheodore@uab.edu
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural