Voltage-gated Potassium Channels in Human Immunodeficiency Virus Type-1 (HIV-1)-associated Neurocognitive Disorders
| Autor: | Dehui Hu, James Keblesh, Huangui Xiong |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
AIDS Dementia Complex
Immunology Neuroscience (miscellaneous) Article Pathogenesis Cognition Immune system Memory medicine Animals Humans Learning Immunology and Allergy Dementia Pharmacology Microglia Long-term potentiation Voltage-gated potassium channel medicine.disease medicine.anatomical_structure Potassium Channels Voltage-Gated Signal transduction Cognition Disorders Psychology Neuroscience Neurocognitive |
| Zdroj: | Journal of Neuroimmune Pharmacology. 4:60-70 |
| ISSN: | 1557-1904 1557-1890 |
| DOI: | 10.1007/s11481-008-9106-6 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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