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Publication Abstract Display
Type: Published Abstract
Title: Neuropsychological ability and regional neuropathology in HIV.
Authors: Moore DJ, Cherner M, Masliah E, Gonzalez R, Carey C, Rippeth J, Marcotte T, Heaton RK, Grant I, and the HNRC Group
Year: 2002
Publication: Journal of the International Neuropsychological Society
Volume: 8 Issue: 2 Pages: 187-188
Abstract:This study examined the relationship between ante mortem neuropsychological (NP) ability and post-mortem neuropathological changes [i.e., HIV encephalitis (HIVE) and a putative measure of neurodegeneration (ND)]. Subjects were 27 individuals with comprehensive NP testing within 18 months of death (median 5 8.5 months). Blind clinical ratings for 7 NP ability domains, as well as an overall global rating, were derived from demographically corrected T-scores of individual NP tests. HIVE was measured by immunolabeling against HIV gp41 envelope protein and was measured in several different brain regions. Additionally, tissue sections were immunolabeled with an antibody against calbindin reflecting the number of calbindin-containing neurons in the frontal cortex and basal ganglia, which has been suggested as a measure of ND in HIV disease. A trend was found between a continuous measure of HIVE and global clinical rating (F(1,25) = 2.7, p = .11, R2 = .10). There were significant associations between the severity of HIVE and NP ratings of learning (F(1,25) = 8.6, p < .01, R2 = .26), abstraction (F(1,25)= 8.1, p < .01, R2 = .27), attention (F(1,25)=5.1, p < .05, R2 = .17) and verbal abilities (F(1,25) = 6.0, p < .05, R2=.20). No relationship was found between the number of calbindin-containing neurons and NP ability. Despite the preliminary nature of this study, these findings support the hypothesis that HIV-related cognitive impairment is associated with the presence and severity of HIVE. Although NP functioning was not related to the number of calbindin-containing neurons, it is uncertain whether this measure reflects true neurodegeneration in this sample because data regarding the density of calbindin-containing neurons in HIV2 individuals is sparse.

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