Glial Cytokines as Neuropathogenic Factors in Hiv-Infection - Pathogenic Similarities to Alzheimers-Disease

Stanley, L. C., Mrak, R. E., Woody, R. C., Perrot, L. J., Zhang, S. X., Marshak, D. R., Nelson, S. J., Griffin, W. S. T. (May 1994) Glial Cytokines as Neuropathogenic Factors in Hiv-Infection - Pathogenic Similarities to Alzheimers-Disease. Journal of Neuropathology and Experimental Neurology, 53 (3). pp. 231-238. ISSN 0022-3069

URL: http://www.ncbi.nlm.nih.gov/pubmed/8176406

Abstract

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.

Item Type: Paper
Uncontrolled Keywords: ACQUIRED IMMUNODEFICIENCY SYNDROME ALZHEIMERS DISEASE GLIA HUMAN IMMUNODEFICIENCY VIRUS INTERLEUKIN-1 S100-BETA TEMPORAL LOBE AMYLOID PRECURSOR PROTEIN CENTRAL NERVOUS-SYSTEM AIDS DEMENTIA COMPLEX ACQUIRED-IMMUNODEFICIENCY-SYNDROME IMMUNE-DEFICIENCY-SYNDROME CELL-PROLIFERATION BRAIN CULTURES INTERLEUKIN-1 IMMUNOREACTIVITY MACROPHAGES
Subjects: diseases & disorders > mental disorders > delirium dementia cognitive disorders > Alzheimer's disease
diseases & disorders > viral diseases > HIV
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > glia cells
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > glia cells
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > glia cells
CSHL Authors:
Communities: CSHL labs
Depositing User: Matt Covey
Date: May 1994
Date Deposited: 26 Jun 2015 20:34
Last Modified: 26 Jun 2015 20:34
Related URLs:
URI: http://repository.cshl.edu/id/eprint/31467

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