ReviewNeurochemical research2019
Scaling Synapses in the Presence of HIV.
Review in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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.
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Who cites it
27 citing papers in PubMed.
- Review
- Microglial reactivity and nodule formation are associated with Synaptodendritic damage in the brains of people with HIV-1.Brain pathology (Zurich, Switzerland) · 2026Article
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- HIV-1 Tat and gp120 as key drivers of neurodegeneration in the central nervous system.Frontiers in microbiology · 2026Review
- Global analysis of excitotoxicity-induced alterations in RNA structure and RNA-protein binding in neurons.iScience · 2025Article
- SIV infection induces alterations in gene expression and loss of interneurons in Rhesus Macaque frontal cortex during early systemic infection.Translational psychiatry · 2025Article
- Levetiracetam Prevents Neurophysiological Changes and Preserves Cognitive Function in the Human Immunodeficiency Virus (HIV)-1 Transactivator of Transcription Transgenic Mouse Model of HIV-Associated Neurocognitive Disorder.The Journal of pharmacology and experimental therapeutics · 2024Article
- Article
- HIV-1 envelope protein gp120 modulation of glutamate effects on cortical neuronal synapses: implications for HIV-1-associated neuropathogenesis.International journal of physiology, pathophysiology and pharmacology · 2023Article
- Influence of HIV infection on cognition and overall intelligence in HIV-infected individuals: advances and perspectives.Frontiers in behavioral neuroscience · 2023Review
- A Rationale and Approach to the Development of Specific Treatments for HIV Associated Neurocognitive Impairment.Microorganisms · 2022Review
- Aberrant Synaptic Pruning in CNS Diseases: A Critical Player in HIV-Associated Neurological Dysfunction?Cells · 2022Review
- Longitudinal trajectories of brain volume in combined antiretroviral therapy treated and untreated simian immunodeficiency virus-infected rhesus macaques.AIDS (London, England) · 2021Article
- GPR18 drives FAAH inhibition-induced neuroprotection against HIV-1 Tat-induced neurodegeneration.Experimental neurology · 2021Article
- Chronic SSRI treatment reverses HIV-1 protein-mediated synaptodendritic damage.Journal of neurovirology · 2021Article
- Mechanisms of neuronal dysfunction in HIV-associated neurocognitive disorders.Cellular and molecular life sciences : CMLS · 2021Review
- Novel Therapeutic Approach for Excitatory/Inhibitory Imbalance in Neurodevelopmental and Neurodegenerative Diseases.Annual review of pharmacology and toxicology · 2021Review
- Neurogranin: A Potential Biomarker of Neurological and Mental Diseases.Frontiers in aging neuroscience · 2020Review
- HIV-1 Tat Length: Comparative and Functional Considerations.Frontiers in microbiology · 2020Article
- Druggable targets of the endocannabinoid system: Implications for the treatment of HIV-associated neurocognitive disorder.Brain research · 2019Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
A defining feature of HIV-associated neurocognitive disorder (HAND) is the loss of excitatory synaptic connections. Synaptic changes that occur during exposure to HIV appear to result, in part, from a homeostatic scaling response. Here we discuss the mechanisms of these changes from the perspective that they might be part of a coping mechanism that reduces synapses to prevent excitotoxicity. In transgenic animals expressing the HIV proteins Tat or gp120, the loss of synaptic markers precedes changes in neuronal number. In vitro studies have shown that HIV-induced synapse loss and cell death are mediated by distinct mechanisms. Both in vitro and animal studies suggest that HIV-induced synaptic scaling engages new mechanisms that suppress network connectivity and that these processes might be amenable to therapeutic intervention. Indeed, pharmacological reversal of synapse loss induced by HIV Tat restores cognitive function. In summary, studies indicate that there are temporal, mechanistic and pharmacological features of HIV-induced synapse loss that are consistent with homeostatic plasticity. The increasingly well delineated signaling mechanisms that regulate synaptic scaling may reveal pharmacological targets suitable for normalizing synaptic function in chronic neuroinflammatory states such as HAND.
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