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030 Brain aging and cardiovascular risk factors in chronic HIV: A longitudinal MRI study
  1. David Jakabek1,2,3,
  2. Caroline D Rae2,3,
  3. Bruce J Brew1,2,3,4 and
  4. Lucette A Cysique1,2,5
  1. 1Departments of Neurology and HIV Medicine, St Vincent’s Hospital, and Peter Duncan Neurosciences Unit, St Vincent’s Centre for Applied Medical Research, Sydney, NSW, Australia
  2. 2Neuroscience Research Australia, Sydney, NSW, Australia
  3. 3Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia
  4. 4Faculty of Medicine, University of Notre Dame, Sydney, NSW, Australia
  5. 5UNSW Psychology, University of New South Wales, Sydney, NSW, Australia


Objectives We aimed to examine the relative contributions of HIV infection, age, and cardiovascular risk factors to subcortical brain atrophy.

Methods Virally suppressed HIV+ participants with low neuropsychological confounds (n = 75) and demographically matched HIV- controls (n = 31) completed baseline and 18-month follow-up MRI scans, neuropsychological evaluation, cardiovascular assessments, and laboratory tests. HIV+ participants were evaluated for HIV associated neurocognitive disorder (HAND). Subcortical volumes were extracted with Freesurfer. Volumetric and shape analyses were conducted using linear mixed-effect models incorporating interactions between age, time, and each of HIV status, HAND status, HIV disease factors, and cardiovascular markers.

Results HIV+ participants had smaller volumes of most structures compared to HIV- participants. Premature aging was evident in the pallidum using volumetric (p = 0.032) and shape analyses. Accelerated aging was observed in the caudate volumes for the more severe HAND subgroup (p = 0.008) and was associated with longer HIV duration for putamen volumes (p = 0.04). Higher CD4 counts had a protective effect on hippocampal volumes in older participants (p = 0.04). Cardiovascular measures were associated with smaller volumes across time for most structures; only the putamen demonstrated accelerated atrophy over time in HIV+ participants with higher cardiovascular risk factors (p = 0.002).

Conclusion The study demonstrates a three-hit model of subcortical injury in HIV+ individuals: HIV-driven atrophy in most subcortical structures; abnormal brain aging and HIV infection synergy in the caudate and pallidum; and cardiovascular-related injury linked to diffuse premature atrophy and emerging accelerated atrophy in the putamen.

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