ReviewCurrent HIV/AIDS reports2026
HIV-1 Tat-driven Glutamate Dysregulation: Implications for Cognitive Impairment in HAND.
Review in Current HIV/AIDS reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The prefrontal cortex as a target of HIV-1 neurotoxicity: molecular mechanisms of viral protein-mediated neurodegeneration and executive dysfunction.Frontiers in cellular neuroscience · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
purpose of reviewHIV-1-associated neurocognitive disorders (HAND) manifest in 15% to 50% of people with HIV, impairing learning and memory and executive function. The chronic generation of HIV-1 Transactivator of transcription (Tat) likely contributes to HAND via direct neuronal toxicity and glial-mediated toxicity. This review summarizes our current understanding of how chronic Tat generation from microglia and astrocytes promote glutamate excitotoxicity. RECENT
findingsIn recent years, the indirect effects of Tat through the activation of glial cells have gained significant interest. This review highlights microglia and astrocytes as HIV-1 reservoirs that release Tat protein in the central nervous system. Specific context is provided on the Tat isoforms and models in the recent literature and their impact on our understanding of the neuronal and glial-mediated effects of Tat on glutamate transmission. Transgenic and transduction models of HIV-1 Tat expression in glia have demonstrated Tat-induced glial activation phenotypes that contribute to dysregulation of glutamate receptors and transporters. Investigating both glial-mediated and direct mechanisms of Tat-potentiated excitotoxicity can identify therapeutic targets that are relevant for HAND.
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Registered trials
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