This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.
Aims and Methods: We are using structural MRI, diffusion tensor imaging (DTI) and spectroscopic imaging (MRSI) to examine the deleterious effects of HIV infection and alcohol abuse?alone and in combination?on brain structure and associated function in a controlled, naturalistic, longitudinal design to model cumulative and progressive effects on the brain of HIV infection and alcohol abuse using four groups: HIV+ with low or high alcohol consumption and HIV- with low or high alcohol consumption. A total of 175 people have entered the study, of which 115 have returned for 1-year follow-up MRI scan. All subjects have had structural MR and DTI scans and a subset have also had an MRSI protocol with variable density spiral sequence to quantify major proton metabolites, Results: Included in the MRSI study were 15 men with HIV+alcoholism, 9 men with HIV alone, 8 men with alcoholism alone (abstinent for 3 to 17 months), and 23 controls. The two HIV groups were matched in T-cell count and were not demented. N-acetylaspartate (NAA), creatine (Cr), and choline (Cho) were measured in the superior parietal-occipital cortex. Metabolites were expressed in absolute units and as the NAA/Cr ratio. Significant group effects were present for NAA and Cr. Only the HIV+alcoholism group was significantly affected, exhibiting a 0.8 standard deviation deficit in NAA and a 1.0 standard deviation deficit in Cr. The deficits were not related to Highly Active Anti-Retroviral Treatment status. Conclusions: Neither HIV infection nor alcoholism independently resulted in parietal-occipital cortical metabolite abnormalities, yet each disease carried a liability that put affected individuals at a heightened risk of neuronal compromise when the diseases were compounded. Further, the use of absolute measures revealed deficits in NAA and creatine that would have gone undetected if these metabolites were expressed as a ratio.
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