Neurologic abnormalities are common in AIDS. While it is clear that CNS infection with HIV may manifest as a subcortical encephalitis, unfortunately, not all patients with AIDS dementia complex reveal this histopathology. This has led to a search for alternative explanations for dementia. In particular, recent emphasis has been placed upon the possible role of neuronal damage in the genesis of AIDS dementia complex. This neuropathologic investigation will examine the extent and nature of grey matter abnormalities in the brains of patients dying with AIDS, and will correlate these with clinical neurologic features. Specifically, this project will utilize autopsy brains from AIDS patients that are histopathologically sorted into 3 groups: HIV encephalitis, aseptic leptomeningitis, and no infectious abnormalities, as well as brains from HIV-negative controls to determine: 1. if HIV infection results in decreased neuronal counts or neuronal atrophy; 2. if there is a pattern of selective vulnerability in neurons undergoing pathologic changes; 3. if abnormal glial responses occur in grey matter and can be correlated with neuronal changes; 4. if CNS glucose transporters show any decrement with HIV infection; and 5. if any detected neuronal abnormalities can be correlated with clinical data, specifically the presence of AIDS dementia complex. The methods entailed in this study are computer-assisted morphometric analysis in concert with histochemistry and immunohistochemistry; immuno-blotting; and polymerase chain reaction.
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Kovitz, C A; Morgello, S (1997) Cerebral glucose transporter expression in HIV infection. Acta Neuropathol (Berl) 94:140-5 |
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