Metabolic and Functional-Studies On Postmortem Human-Brain

Hardy, JA and Dodd, PR (1983) Metabolic and Functional-Studies On Postmortem Human-Brain. Neurochemistry International, 5 3: 253-266. doi:10.1016/0197-0186(83)90027-X


Author Hardy, JA
Dodd, PR
Title Metabolic and Functional-Studies On Postmortem Human-Brain
Journal name Neurochemistry International   Check publisher's open access policy
ISSN 0197-0186
Publication date 1983-01-01
Year available 1983
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1016/0197-0186(83)90027-X
Open Access Status DOI
Volume 5
Issue 3
Start page 253
End page 266
Total pages 14
Publisher PERGAMON-ELSEVIER SCIENCE LTD
Language eng
Abstract Methamphetamine (Meth) use is frequent among HIV-infected persons. Combined HIV and Meth insults may exacerbate neural injury in vulnerable neuroanatomic structures or circuitries in the brain, leading to increased behavioral disturbance and cognitive impairment. While acute and chronic effects of Meth in humans and animal models have been studied for decades, the neurobehavioral effects of Meth in the context of HIV infection are much less explored. In-depth understanding of the scope of neurobehavioral phenotypes and mechanisms in HIV/Meth intersection is needed. The present report summarizes published research findings, as well as unpublished data, in humans and animal models with regard to neurobehavioral disturbance, neuroimaging, and neuropathology, and in vitro experimental systems, with an emphasis on findings emerging from the National Institute on Drug Abuse (NIDA) funded Translational Methamphetamine AIDS Research Center (TMARC). Results from human studies and animal (primarily HIV-1 gp120 transgenic mouse) models thus far suggest that combined HIV and Meth insults increase the likelihood of neural injury in the brain. The neurobehavioral effects include cognitive impairment and increased tendencies toward impaired behavioral inhibition and social cognition. These impairments are relevant to behaviors that affect personal and social risks, e.g. worse medication adherence, riskier behaviors, and greater likelihood of HIV transmission. The underlying mechanisms may include electrochemical changes in neuronal circuitries, injury to white matter microstructures, synaptodendritic damage, and selective neuronal loss. Utilization of research methodologies that are valid across species is instrumental in generating new knowledge with clinical translational value.
Keyword Cognition
Inhibition
Neuroimaging
Neuropathology
Tat
gp120
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID R01 MH105319
P50 DA026306
R01 AG043384
T32 DA031098
R13 DA035084
R01 MH096648
P30 MH062512
P01 DA012065
Institutional Status Unknown

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collection: ResearcherID Downloads - Archived
 
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