ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2009
Voltage-gated potassium channels in human immunodeficiency virus type-1 (HIV-1)-associated neurocognitive disorders.
Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Single-Cell Multi-Modal Differential Analysis of the Human Neo-Cortex in HIV Infection Reveals Similarities with Hallmarks of Alzheimer's Disease.Research square · 2025Article
- Simian immunodeficiency virus transiently increases brain temperature in rhesus monkeys: detection with magnetic resonance spectroscopy thermometry.Magnetic resonance in medicine · 2019Article
- G protein-coupled and ATP-sensitive inwardly rectifying potassium ion channels are essential for HIV entry.Scientific reports · 2019Article
- Target of HIV-1 Envelope Glycoprotein gp120-Induced Hippocampal Neuron Damage: Role of Voltage-Gated K(+) Channel Kv2.1.Viral immunology · 2015Article
- Facial emotion recognition impairments are associated with brain volume abnormalities in individuals with HIV.Neuropsychologia · 2015Article
- Plasma gelsolin protects HIV-1 gp120-induced neuronal injury via voltage-gated K+ channel Kv2.1.Molecular and cellular neurosciences · 2013Article
- Distinct modifications in Kv2.1 channel via chemokine receptor CXCR4 regulate neuronal survival-death dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Towards therapeutic applications of arthropod venom k(+)-channel blockers in CNS neurologic diseases involving memory acquisition and storage.Journal of toxicology · 2012Article
- HIV-1gp120 induces neuronal apoptosis through enhancement of 4-aminopyridine-senstive outward K+ currents.PloS one · 2011Article
- Involvement of the 4-aminopyridine-sensitive transient A-type K+ current in macrophage-induced neuronal injury.The European journal of neuroscience · 2010Article
- Nanobiology for the pharmacology of cellular ion channels.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2009Article
Corrections and comments
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Authors and funding
3 authors.
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Abstract
Human immunodeficiency virus type-1 (HIV-1)-associated dementia (HAD), a severe form of HIV-associated neurocognitive disorders (HAND), describes the cognitive impairments and behavioral disturbances which afflict many HIV-infected individuals. Although the precise mechanism leading to HAD is incompletely understood, it is commonly accepted its progression involves a critical mass of infected and activated mononuclear phagocytes (brain perivascular macrophages and microglia) releasing immune and viral products in the brain. These cellular and viral products induce neuronal dysfunction and injury via various signaling pathways. Emerging evidence indicates voltage-gated potassium (K(v)) channels, key regulators of cell excitability and animal behavior (learning and memory), are involved in the pathogenesis of HAD/HAND. Here we survey the literature and find that HAD-related alterations in cellular and viral products can increase neuronal K(v) channel activity, leading to neuronal dysfunction and cognitive deficits. Thus, neuronal K(v) channels may be a new target in the effort to develop therapies for HAD and perhaps other inflammatory neurodegenerative disorders.
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