- Lifelong antiretroviral therapy extends lifespan yet HAND persists with ageing, raising concern for co-development of Alzheimer's disease despite viral suppression.
- HAND and AD share mechanisms: chronic neuroinflammation, glial dysfunction, and progressive neurodegeneration, with microglial activation driving persistent proinflammatory neurotoxins.
- Persistent viral reservoirs and low level viral protein expression disrupt glial homeostasis, increasing oxidative stress, tau hyperphosphorylation, and synaptic damage.
Neurosci Biobehav Rev. 2026 Aug 29;190:106932. doi: 10.1016/j.neubiorev.2026.106932. Online ahead of print.
ABSTRACT
Lifelong antiretroviral therapy extends the lifespan of individuals with human immunodeficiency virus (HIV). However, HIV-associated neurocognitive disorders (HAND) remain with age-linked comorbidities. Despite viral suppression, the co-development of Alzheimer’s disease (AD) remains a concern. Both HAND and AD share key mechanisms, including chronic neuroinflammation, glial dysfunction, and progressive neurodegeneration. Microglial activation is a key contributor that generates persistent proinflammatory neurotoxins, promoting amyloid-β aggregation, disrupting clearance, and accelerating neurodegeneration. Persistent viral reservoirs and low-level viral protein expression disrupt glial homeostasis, enhancing oxidative stress, tau hyperphosphorylation, and synaptic damage in the brain. This review highlights the intersections between both disorders and discusses emerging rodent models to investigate convergent pathways with the goal of improving therapeutic strategies to preserve cognitive health.
PMID:42667832 | DOI:10.1016/j.neubiorev.2026.106932
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