Vishal Samboju1, Yann Cobigo1, Robert Paul2, Georges Naasan1,3,4, Madeline Hillis1, Torie Tsuei1, Shireen Javandel1, Victor Valcour1,3, Benedetta Milanini1. 1. Department of Neurology, Memory and Aging Center, University of California San Francisco, CA. 2. Missouri Institute of Mental Health, University of Missouri, St. Louis, MO. 3. Global Brain Health Institute, University of California, San Francisco, CA;and. 4. Department of Neurology, The Barbara and Maurice Deanne Center for Wellness and Cognitive Health, Icahn School of Medicine, Mount Sinai, NY.
Abstract
BACKGROUND: Mild cognitive difficulties and progressive brain atrophy are observed in older people living with HIV (PLWH) despite persistent viral suppression. Whether cerebrovascular disease (CVD) risk factors and white matter hyperintensity (WMH) volume correspond to the observed progressive brain atrophy is not well understood. METHODS: Longitudinal structural brain atrophy rates and WMH volume were examined among 57 HIV-infected participants and 40 demographically similar HIV-uninfected controls over an average (SD) of 3.4 (1.7) years. We investigated associations between CVD burden (presence of diabetes, hypertension, hyperlipidemia, obesity, smoking history, and atrial fibrillation) and WMH with atrophy over time. RESULTS: The mean (SD) age was 64.8 (4.3) years for PLWH and 66.4 (3.2) years for controls. Participants and controls were similar in age and sex (P > 0.05). PLWH were persistently suppressed (VL <375 copies/mL with 93% <75 copies/mL). The total number of CVD risk factors did not associate with atrophy rates in any regions of interests examined; however, body mass index independently associated with progressive atrophy in the right precentral gyrus (β = -0.30; P = 0.023), parietal lobe (β = -0.28; P = 0.030), and frontal lobe atrophy (β = -0.27; P = 0.026) of the HIV-infected group. No associations were found in the HIV-uninfected group. In both groups, baseline WMH was associated with progressive atrophy rates bilaterally in the parietal gray in the HIV-infected group (β = -0.30; P = 0.034) and the HIV-uninfected participants (β = -0.37; P = 0.033). CONCLUSIONS: Body mass index and WMH are associated with atrophy in selective brain regions. However, CVD burden seems to partially contribute to progressive brain atrophy in older individuals regardless of HIV status, with similar effect sizes. Thus, CVD alone is unlikely to explain accelerated atrophy rates observed in virally suppressed PLWH. In older individuals, addressing modifiable CVD risk factors remains important to optimize brain health.
BACKGROUND: Mild cognitive difficulties and progressive brain atrophy are observed in older people living with HIV (PLWH) despite persistent viral suppression. Whether cerebrovascular disease (CVD) risk factors and white matter hyperintensity (WMH) volume correspond to the observed progressive brain atrophy is not well understood. METHODS: Longitudinal structural brain atrophy rates and WMH volume were examined among 57 HIV-infected participants and 40 demographically similar HIV-uninfected controls over an average (SD) of 3.4 (1.7) years. We investigated associations between CVD burden (presence of diabetes, hypertension, hyperlipidemia, obesity, smoking history, and atrial fibrillation) and WMH with atrophy over time. RESULTS: The mean (SD) age was 64.8 (4.3) years for PLWH and 66.4 (3.2) years for controls. Participants and controls were similar in age and sex (P > 0.05). PLWH were persistently suppressed (VL <375 copies/mL with 93% <75 copies/mL). The total number of CVD risk factors did not associate with atrophy rates in any regions of interests examined; however, body mass index independently associated with progressive atrophy in the right precentral gyrus (β = -0.30; P = 0.023), parietal lobe (β = -0.28; P = 0.030), and frontal lobe atrophy (β = -0.27; P = 0.026) of the HIV-infected group. No associations were found in the HIV-uninfected group. In both groups, baseline WMH was associated with progressive atrophy rates bilaterally in the parietal gray in the HIV-infected group (β = -0.30; P = 0.034) and the HIV-uninfected participants (β = -0.37; P = 0.033). CONCLUSIONS: Body mass index and WMH are associated with atrophy in selective brain regions. However, CVD burden seems to partially contribute to progressive brain atrophy in older individuals regardless of HIV status, with similar effect sizes. Thus, CVD alone is unlikely to explain accelerated atrophy rates observed in virally suppressed PLWH. In older individuals, addressing modifiable CVD risk factors remains important to optimize brain health.
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