Abstract

HIV-1 associated dementia (HAD) is a metabolic encephalopathy induced by viral infection and fueled by immune activation of brain mononuclear phagocytes (perivascular and parenchymal macrophages and microglia). These same cells serve as reservoirs for persistent infection and sources for soluble neurotoxins. Neurologic impairments are manifested by cognitive, behavioral, and motor abnormalities that occur years after viral exposure and are associated with depletion of CD4+ T lymphocytes and high viral loads. Improvements in antiretroviral and adjunctive therapies have decreased HAD incidence, but cognitive dysfunction remains a cause of morbidity in many infected persons.

Original languageEnglish (US)
Pages (from-to)358-368
Number of pages11
JournalAIDS Reader
Volume12
Issue number8
StatePublished - Aug 1 2002

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Dementia
HIV-1
Metabolic Brain Diseases
Neurotoxins
Microglia
Virus Diseases
Phagocytes
Viral Load
Nervous System
Macrophages
Morbidity
T-Lymphocytes
Incidence
Brain
Infection
Cognitive Dysfunction
Therapeutics

Keywords

  • HIV-1-associated cognitive dysfunction
  • HIV-1-associated dementia
  • HIV/AIDS
  • Macrophages
  • Microglia
  • Neurotoxins

ASJC Scopus subject areas

  • Infectious Diseases

Cite this

HIV-1-associated dementia : A basic science and clinical perspective. / Diesing, Thomas S.; Swindells, Susan; Gelbard, Harris; Gendelman, Howard Eliot.

In: AIDS Reader, Vol. 12, No. 8, 01.08.2002, p. 358-368.

Research output: Contribution to journalReview article

Diesing, Thomas S. ; Swindells, Susan ; Gelbard, Harris ; Gendelman, Howard Eliot. / HIV-1-associated dementia : A basic science and clinical perspective. In: AIDS Reader. 2002 ; Vol. 12, No. 8. pp. 358-368.
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