作者:
DOI: 10.4137/RRT.S1041
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摘要: HIV-1-associated dementia (HAD) describes the cognitive impairments and behavioral disturbances which afflict many HIV-infected individuals. Although incidence of HAD has decreased significantly in era HAART, it remains a significant complication HIV-1 infection as patients with acquired immune deficient syndrome (AIDS) live longer, antiretroviral drugs remain unable to effectively cross blood-brain barrier (BBB), resistance grows due viral strain mutation. precise mechanism leading is incompletely understood, commonly accepted its progression involves critical mass infected activated mononuclear phagocytes (MP; brain perivascular macrophages microglia) releasing products brain. These cellular induce neuronal dysfunction injury via various signaling pathways. Emerging evidence indicates that voltage-gated potassium (K(v)) channels, key regulators cell excitability animal behavior (learning memory), are involved pathogenesis HAD/HAND. Here we survey literature find related alterations can alter MP K(v) channel activity, deficits. Thus, channels may be new target effort develop therapies for perhaps other inflammatory neurodegenerative disorders.