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Brain Sci. 2016, 6(3), 23; doi:10.3390/brainsci6030023

Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198-5880, USA
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Author to whom correspondence should be addressed.
Academic Editor: Donna Gruol
Received: 2 April 2016 / Revised: 12 July 2016 / Accepted: 20 July 2016 / Published: 22 July 2016
(This article belongs to the Special Issue Advances in Neuroimmunology)
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Abstract

Oligodendrocytes wrap neuronal axons to form myelin, an insulating sheath which is essential for nervous impulse conduction along axons. Axonal myelination is highly regulated by neuronal and astrocytic signals and the maintenance of myelin sheaths is a very complex process. Oligodendrocyte damage can cause axonal demyelination and neuronal injury, leading to neurological disorders. Demyelination in the cerebrum may produce cognitive impairment in a variety of neurological disorders, including human immunodeficiency virus type one (HIV-1)-associated neurocognitive disorders (HAND). Although the combined antiretroviral therapy has markedly reduced the incidence of HIV-1-associated dementia, a severe form of HAND, milder forms of HAND remain prevalent even when the peripheral viral load is well controlled. HAND manifests as a subcortical dementia with damage in the brain white matter (e.g., corpus callosum), which consists of myelinated axonal fibers. How HIV-1 brain infection causes myelin injury and resultant white matter damage is an interesting area of current HIV research. In this review, we tentatively address recent progress on oligodendrocyte dysregulation and HAND pathogenesis. View Full-Text
Keywords: HIV-1; dementia; oligodendrocyte; myelin sheath HIV-1; dementia; oligodendrocyte; myelin sheath
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Liu, H.; Xu, E.; Liu, J.; Xiong, H. Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders. Brain Sci. 2016, 6, 23.

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