This project was undertaken to elucidate biochemical and immunological aspects of myelin disorders associated with neuro-AIDS including myelin pallor, vacuolar myelopathy and multifocal demyelination in the CNS as well as demyelinating peripheral neuropathy. Postmortem CNS tissue from AIDS patients is being analyzed for quantitative and qualitative alterations of myelin proteins, including myelin-associated glycoprotein, myelin basic protein, proteolipid protein and 2'3'-cyclic nucleotide 3'- phosphodiesterase. The biochemical results are being correlated with histological and immunocytochemical observations made by our collaborators at Johns Hopkins University on adjacent sections of tissue. So far immunocytochemical staining of white matter of AIDS CNS has not suggested substantial loss of myelin proteins in areas where there is prominent myelin pallor, but a definitive conclusion on this must await the results of our quantitative biochemical studies currently in progress on AIDS cases with dementia in which myelin abnormalities are most common. It has been suggested that some of the myelin abnormalities in AIDS, and other neurological diseases caused by retroviruses, may be related to autoimmune phenomena. However, Western blotting experiments done this year have not revealed antibodies to proteins of CNS or PNS myelin in 10 sera from rabbits with HTLV-1 or 6 monkeys infected with SIV. In our previous studies on antibodies to gangliosides in the inflammatory peripheral neuropathies, one patient with high levels of serum antibodies to G-D16-ganglioside was HIV-positive. Thus far, we have not detected anti-ganglioside antibodies in a limited number of additional AIDS patients with neuropathy.
