James H Cole1,2, Matthan W A Caan3, Jonathan Underwood4, Davide De Francesco5, Rosan A van Zoest6, Ferdinand W N M Wit6,7, Henk J M M Mutsaerts3,8, Rob Leech1, Gert J Geurtsen9, Peter Portegies10,11, Charles B L M Majoie3, Maarten F Schim van der Loeff12,13, Caroline A Sabin5, Peter Reiss6,7, Alan Winston4, David J Sharp1. 1. Computational, Cognitive and Computational Neuroimaging Laboratory, Division of Brain Sciences, Imperial College London. 2. Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, United Kingdom. 3. Department of Radiology and Nuclear Medicine, Academic Medical Center, Amsterdam, The Netherlands. 4. Division of Infectious Diseases, Imperial College London. 5. Department of Infection and Population Health, University College London, United Kingdom. 6. Department of Global Health, Academic Medical Center, Amsterdam Institute for Global Health and Development. 7. Dutch HIV Monitoring Foundation, Amsterdam, The Netherlands. 8. Kate Gleason College of Engineering, Rochester Institute of Technology, New York. 9. Department of Medical Psychology, Academic Medical Center. 10. Department of Neurology, OLVG Hospital. 11. Department of Neurology, Academic Medical Center. 12. Department of Infectious Diseases, Public Health Service of Amsterdam. 13. Department of Infectious Diseases, Center for Immunity and Infection Amsterdam, Academic Medical Center, University of Amsterdam, The Netherlands.
Abstract
Background: Despite successful antiretroviral therapy, people living with human immunodeficiency virus (PLWH) experience higher rates of age-related morbidity, including abnormal brain structure, brain function, and cognitive impairment. This has raised concerns that PLWH may experience accelerated aging-related brain pathology. Methods: We performed a multicenter longitudinal study of 134 virologically suppressed PLWH (median age, 56.0 years) and 79 demographically similar human immunodeficiency virus (HIV)-negative controls (median age, 57.2 years). To measure cognitive performance and brain pathology, we conducted detailed neuropsychological assessments and multimodality neuroimaging (T1-weighted, T2-weighted, diffusion magnetic resonance imaging [MRI], resting-state functional MRI, spectroscopy, arterial spin labeling) at baseline and at 2 years. Group differences in rates of change were assessed using linear mixed effects models. Results: One hundred twenty-three PLWH and 78 HIV-negative controls completed longitudinal assessments (median interval, 1.97 years). There were no differences between PLWH and HIV-negative controls in age, sex, years of education, smoking or alcohol use. At baseline, PLWH had poorer global cognitive performance (P < .01), lower gray matter volume (P = .04), higher white matter hyperintensity load (P = .02), abnormal white matter microstructure (P < .005), and greater brain-predicted age difference (P = .01). Longitudinally, there were no significant differences in rates of change in any neuroimaging measure between PLWH and HIV-negative controls (P > .1). Cognitive performance was longitudinally stable in both groups. Conclusions: We found no evidence that middle-aged PLWH, when receiving successful treatment, are at increased risk of accelerated aging-related brain changes or cognitive decline over 2 years.
Background: Despite successful antiretroviral therapy, people living with human immunodeficiency virus (PLWH) experience higher rates of age-related morbidity, including abnormal brain structure, brain function, and cognitive impairment. This has raised concerns that PLWH may experience accelerated aging-related brain pathology. Methods: We performed a multicenter longitudinal study of 134 virologically suppressed PLWH (median age, 56.0 years) and 79 demographically similar human immunodeficiency virus (HIV)-negative controls (median age, 57.2 years). To measure cognitive performance and brain pathology, we conducted detailed neuropsychological assessments and multimodality neuroimaging (T1-weighted, T2-weighted, diffusion magnetic resonance imaging [MRI], resting-state functional MRI, spectroscopy, arterial spin labeling) at baseline and at 2 years. Group differences in rates of change were assessed using linear mixed effects models. Results: One hundred twenty-three PLWH and 78 HIV-negative controls completed longitudinal assessments (median interval, 1.97 years). There were no differences between PLWH and HIV-negative controls in age, sex, years of education, smoking or alcohol use. At baseline, PLWH had poorer global cognitive performance (P < .01), lower gray matter volume (P = .04), higher white matter hyperintensity load (P = .02), abnormal white matter microstructure (P < .005), and greater brain-predicted age difference (P = .01). Longitudinally, there were no significant differences in rates of change in any neuroimaging measure between PLWH and HIV-negative controls (P > .1). Cognitive performance was longitudinally stable in both groups. Conclusions: We found no evidence that middle-aged PLWH, when receiving successful treatment, are at increased risk of accelerated aging-related brain changes or cognitive decline over 2 years.
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