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M9460659.TXT
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1994-06-25
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Document 0659
DOCN M9460659
TI Glial cytokines as neuropathogenic factors in HIV infection: pathogenic
similarities to Alzheimer's disease.
DT 9408
AU Stanley LC; Mrak RE; Woody RC; Perrot LJ; Zhang S; Marshak DR; Nelson
SJ; Griffin WS; Department of Pediatrics, University of Arkansas for
Medical; Sciences, Little Rock.
SO J Neuropathol Exp Neurol. 1994 May;53(3):231-8. Unique Identifier :
AIDSLINE MED/94231204
AB The mechanisms by which human immunodeficiency virus (HIV) infection
provokes progressive neurodegeneration and dementia in acquired
immunodeficiency syndrome (AIDS) remain obscure. In HIV-infected (HIV+)
individuals, we found that the brain cells preferentially infected by
HIV, viz. the microglia, were abundant, activated, and intensely
immunopositive for interleukin-1 alpha (IL-1 alpha), an immune
response-generated cytokine that increases the synthesis and processing
of beta-amyloid precursor proteins (beta-APP) and promotes proliferation
and activation of astroglia. We also found an increase in the number of
activated astroglia expressing elevated levels of S100 beta, a cytokine
that increases intraneuronal calcium levels and promotes excessive
growth of neuronal processes (neurites). These glial changes were
accompanied by increased expression of beta-APP immunoreaction product
in neurons and overgrown (dystrophic) neurites. In addition, some
neurons contained monoclonal antibody Tau-2 immunopositive,
neurofibrillary tangle-like structures. Our findings provide evidence
that glial activation with increased expression of IL-1 alpha and S100
beta may be important in the neuropathogenesis of AIDS dementia. We
propose that HIV infection promotes excessive microglial IL-1 alpha
expression with consequent astrogliosis and increased expression of S100
beta. Overexpression of these two cytokines may then be involved in AIDS
neuropathogenesis by inducing gliosis, growth of dystrophic neurites,
and calcium-mediated neuronal cell loss in AIDS.
DE tau Proteins/METABOLISM Adult Alzheimer's
Disease/*METABOLISM/PATHOLOGY Amyloid beta-Protein Precursor/METABOLISM
Brain/*METABOLISM/PATHOLOGY Female Human HIV
Infections/*METABOLISM/PATHOLOGY HIV
Seropositivity/METABOLISM/PATHOLOGY Interleukin-1/*METABOLISM Male
Microglia/*METABOLISM/PATHOLOGY Nerve Tissue Protein S 100/METABOLISM
Support, U.S. Gov't, P.H.S. JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).