BACKGROUND: Accurate prediction of longitudinal changes in cognitive function would potentially allow for targeted intervention in those at greatest risk of cognitive decline. We sought to build a multivariate model using volumetric neuroimaging data alone to accurately predict cognitive function. METHODS: Volumetric T1-weighted neuroimaging data from virally suppressed HIV-positive individuals from the CHARTER cohort (n = 139) were segmented into gray and white matter and spatially normalized before entering into machine learning models. Prediction of cognitive function at baseline and longitudinally was determined using leave-one-out cross-validation. In addition, a multivariate model of brain aging was used to measure the deviation of apparent brain age from chronological age and assess its relationship with cognitive function. RESULTS: Cognitive impairment, defined using the global deficit score, was present in 37.4%. However, it was generally mild and occurred more commonly in those with confounding comorbidities (P < 0.001). Although multivariate prediction of cognitive impairment as a dichotomous variable at baseline was poor (area under the receiver operator curve 0.59), prediction of the global T-score was better than a comparable linear model (adjusted R = 0.08, P < 0.01 vs. adjusted R = 0.01, P = 0.14). Accurate prediction of longitudinal changes in cognitive function was not possible (P = 0.82). Brain-predicted age exceeded chronological age by mean (95% confidence interval) 1.17 (-0.14 to 2.53) years but was greatest in those with confounding comorbidities [5.87 (1.74 to 9.99) years] and prior AIDS [3.03 (0.00 to 6.06) years]. CONCLUSION: Accurate prediction of cognitive impairment using multivariate models using only T1-weighted data was not achievable, which may reflect the small sample size, heterogeneity of the data, or that impairment was usually mild.
BACKGROUND: Accurate prediction of longitudinal changes in cognitive function would potentially allow for targeted intervention in those at greatest risk of cognitive decline. We sought to build a multivariate model using volumetric neuroimaging data alone to accurately predict cognitive function. METHODS: Volumetric T1-weighted neuroimaging data from virally suppressed HIV-positive individuals from the CHARTER cohort (n = 139) were segmented into gray and white matter and spatially normalized before entering into machine learning models. Prediction of cognitive function at baseline and longitudinally was determined using leave-one-out cross-validation. In addition, a multivariate model of brain aging was used to measure the deviation of apparent brain age from chronological age and assess its relationship with cognitive function. RESULTS: Cognitive impairment, defined using the global deficit score, was present in 37.4%. However, it was generally mild and occurred more commonly in those with confounding comorbidities (P < 0.001). Although multivariate prediction of cognitive impairment as a dichotomous variable at baseline was poor (area under the receiver operator curve 0.59), prediction of the global T-score was better than a comparable linear model (adjusted R = 0.08, P < 0.01 vs. adjusted R = 0.01, P = 0.14). Accurate prediction of longitudinal changes in cognitive function was not possible (P = 0.82). Brain-predicted age exceeded chronological age by mean (95% confidence interval) 1.17 (-0.14 to 2.53) years but was greatest in those with confounding comorbidities [5.87 (1.74 to 9.99) years] and prior AIDS [3.03 (0.00 to 6.06) years]. CONCLUSION: Accurate prediction of cognitive impairment using multivariate models using only T1-weighted data was not achievable, which may reflect the small sample size, heterogeneity of the data, or that impairment was usually mild.
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