Potentiation of excitotoxicity in HIV-1-associated Dementia and the significance of glutaminase

Nathan B. Erdmann, Nicholas P. Whitney, Jialin C Zheng

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

HIV-1-associated Dementia (HAD) is a significant consequence of HIV infection. Although multiple inflammatory factors contribute to this chronic, progressive dementia, excitotoxic damage appears to be an underlying mechanism in the neurodegenerative process. Excitotoxicity is a cumulative effect of multiple processes occurring in the CNS during HAD. The overstimulation of glutamate receptors, an increased vulnerability of neurons, and disrupted astrocyte support each potentiate excitotoxic damage to neurons. Recent evidence suggests that poorly controlled generation of glutamate by phosphate-activated glutaminase may contribute to the neurotoxic state typical of HAD as well as other neurodegenerative disorders. Glutaminase converts glutamine, a widely available substrate throughout the CNS to glutamate. Inflammatory conditions may precipitate unregulated activity of glutaminase, a potentially important mechanism in HAD pathogenesis.

Original languageEnglish (US)
Pages (from-to)315-328
Number of pages14
JournalClinical Neuroscience Research
Volume6
Issue number5
DOIs
StatePublished - Dec 1 2006

Fingerprint

Glutaminase
Dementia
HIV-1
Glutamic Acid
Neurons
Glutamate Receptors
Glutamine
Astrocytes
Neurodegenerative Diseases
HIV Infections

Keywords

  • Excitotoxicity
  • Glutamate
  • Glutaminase
  • HIV-1-associated dementia
  • Macrophage
  • Neurodegeneration

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

Cite this

Potentiation of excitotoxicity in HIV-1-associated Dementia and the significance of glutaminase. / Erdmann, Nathan B.; Whitney, Nicholas P.; Zheng, Jialin C.

In: Clinical Neuroscience Research, Vol. 6, No. 5, 01.12.2006, p. 315-328.

Research output: Contribution to journalArticle

@article{0bf52a10bf454cceb784b44ddc88f361,
title = "Potentiation of excitotoxicity in HIV-1-associated Dementia and the significance of glutaminase",
abstract = "HIV-1-associated Dementia (HAD) is a significant consequence of HIV infection. Although multiple inflammatory factors contribute to this chronic, progressive dementia, excitotoxic damage appears to be an underlying mechanism in the neurodegenerative process. Excitotoxicity is a cumulative effect of multiple processes occurring in the CNS during HAD. The overstimulation of glutamate receptors, an increased vulnerability of neurons, and disrupted astrocyte support each potentiate excitotoxic damage to neurons. Recent evidence suggests that poorly controlled generation of glutamate by phosphate-activated glutaminase may contribute to the neurotoxic state typical of HAD as well as other neurodegenerative disorders. Glutaminase converts glutamine, a widely available substrate throughout the CNS to glutamate. Inflammatory conditions may precipitate unregulated activity of glutaminase, a potentially important mechanism in HAD pathogenesis.",
keywords = "Excitotoxicity, Glutamate, Glutaminase, HIV-1-associated dementia, Macrophage, Neurodegeneration",
author = "Erdmann, {Nathan B.} and Whitney, {Nicholas P.} and Zheng, {Jialin C}",
year = "2006",
month = "12",
day = "1",
doi = "10.1016/j.cnr.2006.09.009",
language = "English (US)",
volume = "6",
pages = "315--328",
journal = "Clinical Neuroscience Research",
issn = "1566-2772",
publisher = "Elsevier BV",
number = "5",

}

TY - JOUR

T1 - Potentiation of excitotoxicity in HIV-1-associated Dementia and the significance of glutaminase

AU - Erdmann, Nathan B.

AU - Whitney, Nicholas P.

AU - Zheng, Jialin C

PY - 2006/12/1

Y1 - 2006/12/1

N2 - HIV-1-associated Dementia (HAD) is a significant consequence of HIV infection. Although multiple inflammatory factors contribute to this chronic, progressive dementia, excitotoxic damage appears to be an underlying mechanism in the neurodegenerative process. Excitotoxicity is a cumulative effect of multiple processes occurring in the CNS during HAD. The overstimulation of glutamate receptors, an increased vulnerability of neurons, and disrupted astrocyte support each potentiate excitotoxic damage to neurons. Recent evidence suggests that poorly controlled generation of glutamate by phosphate-activated glutaminase may contribute to the neurotoxic state typical of HAD as well as other neurodegenerative disorders. Glutaminase converts glutamine, a widely available substrate throughout the CNS to glutamate. Inflammatory conditions may precipitate unregulated activity of glutaminase, a potentially important mechanism in HAD pathogenesis.

AB - HIV-1-associated Dementia (HAD) is a significant consequence of HIV infection. Although multiple inflammatory factors contribute to this chronic, progressive dementia, excitotoxic damage appears to be an underlying mechanism in the neurodegenerative process. Excitotoxicity is a cumulative effect of multiple processes occurring in the CNS during HAD. The overstimulation of glutamate receptors, an increased vulnerability of neurons, and disrupted astrocyte support each potentiate excitotoxic damage to neurons. Recent evidence suggests that poorly controlled generation of glutamate by phosphate-activated glutaminase may contribute to the neurotoxic state typical of HAD as well as other neurodegenerative disorders. Glutaminase converts glutamine, a widely available substrate throughout the CNS to glutamate. Inflammatory conditions may precipitate unregulated activity of glutaminase, a potentially important mechanism in HAD pathogenesis.

KW - Excitotoxicity

KW - Glutamate

KW - Glutaminase

KW - HIV-1-associated dementia

KW - Macrophage

KW - Neurodegeneration

UR - http://www.scopus.com/inward/record.url?scp=33845214060&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845214060&partnerID=8YFLogxK

U2 - 10.1016/j.cnr.2006.09.009

DO - 10.1016/j.cnr.2006.09.009

M3 - Article

VL - 6

SP - 315

EP - 328

JO - Clinical Neuroscience Research

JF - Clinical Neuroscience Research

SN - 1566-2772

IS - 5

ER -