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Area of Science:

  • Neuroscience
  • Neuroimaging
  • Aging Research

Background:

  • Human Immunodeficiency Virus (HIV) infection and cocaine use (CU) are independently associated with cognitive deficits and brain abnormalities.
  • The combined impact of HIV and CU on brain aging and cognitive function remains incompletely understood.

Purpose of the Study:

  • To investigate the relationship between comorbid HIV and CU and accelerated brain aging.
  • To examine how the brain age gap (BAG) relates to neurocognitive impairment (NCI) in individuals with HIV and/or CU.
  • To identify specific brain structural changes associated with comorbid HIV and CU.

Main Methods:

  • Trained a morphometry-based brain-age model using Gaussian Process Regression on Human Connectome Project-Aging (HCP-A) data.
  • Applied the model to an independent cohort with varying HIV/CU burden (HIV-/CU-, one disorder, HIV+/CU+).
  • Analyzed brain age gap (BAG) in relation to comorbidity burden and NCI, controlling for covariates; used SHapley Additive exPlanation (SHAP) for network-level analysis.

Main Results:

  • A dose-dependent effect of comorbidity burden on BAG was observed, with the HIV+/CU+ group exhibiting the largest BAG.
  • Increased BAG was significantly associated with a higher likelihood of NCI.
  • BAG partially mediated the association between comorbidity burden and NCI, with a stronger effect in the dual-disorder group.

Conclusions:

  • Comorbid HIV and CU are associated with accelerated structural brain aging.
  • The brain age gap may serve as a biomarker for brain alterations linking comorbid HIV/CU to cognitive impairment.
  • Identifying network-specific contributions to BAG could inform targeted interventions for individuals with comorbid HIV and CU.