Researchers examine the mechanisms responsible for the increased risk of neurocognitive impairment in HIV patients and explore potential treatments.
By Dr. Liji Thomas, MDOct 12 2023Reviewed by Benedette Cuffari, M.Sc. People living with human immunodeficiency virus infection struggle with chronic health conditions, among which include neurocognitive impairment . A recent paper in Nature Reviews Neurology examines the mechanisms responsible for the increased risk of NCI among PLWH and explores potential treatments.
Despite ART, latent infection persists, especially in the brain, with the release of viral proteins. These may cause neuronal degeneration, thereby leading to NCI, which affects 30-50% of PLWH. HIV-associated NCI may reduce adherence to ART, impair attention, concentration, memory, and cognitive function, cause loss of independence, and shorten life.
NCI risk increases with age, lower CD4+ counts , hepatitis C virus infection , comorbidities , lower nadir CD4+ counts , and current ART . A related phenomenon is chronic immune activation, even with sustained ART. Viral RNA and proteins are found in exosomes from infected cells, which alter the function of uninfected immune cells to trigger pro-inflammatory pathways.
Indirect neurotoxicity Brain macrophages and microglia with latent HIV release excitatory substances like quinolinic acid at toxic levels, thereby exciting neuronal glutamate receptors and resulting in memory loss. These immune cells also release inflammatory cytokines, which is exacerbated by ART-induced inflammation.
The activation of the NLRP3 inflammasome is documented in HIV, even with viral suppression. In response to danger signals like oxidative molecules and lysosomal disruption, this inflammasome releases inflammatory chemicals like interleukin 1β and IL-18, which reduces synaptic neurotransmitters, impairs structural and functional growth of neurons, and triggers pyroptosis. Chronic neuroinflammation also exposes the brain to degenerative injury.
Potential pharmacological interventions There are no approved pharmacological treatments for NCI. Some potential drug interventions include human growth hormone-releasing hormone analogs like tesamorelin and phosphatidylinositol-glycan-specific phospholipase D . Tesamorelin restores GH secretion, stimulates brain blood flow, blocks oxidative damage, and promotes neurogenesis and synapse growth through its stimulation of insulin-like growth factor 1 .
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