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Neuronal Injury, White Matter Disease, and Neurotrophic Factors 

Neuronal Injury, White Matter Disease, and Neurotrophic Factors
Neuronal Injury, White Matter Disease, and Neurotrophic Factors

T. Dianne Langford

, Ian Paul Everall

, and Eliezer Masliah

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date: 17 June 2019

Abstract: The patterns of neurodegeneration in AIDS patients, paying special attention to neuronal injury, white matter disease, and the potential role of neurotrophic factors are reviewed. On the cellular level, there is evidence that neuronal damage in AIDS might start in synapses and dendrites and then spread to the rest of the neuron, leading to cell death by apoptosis. Anatomically, neurodegeneration affects primarily the striato-cortical, cortico-cortical, and limbic intrinsic/inhibitory circuitries. Whether these circuitries are affected simultaneously or as part of an anatomical progression is unknown. Differences in the relative levels of specific receptors across neuronal populations may influence their vulnerability to distinct HIV-related neurotoxins. The emergence of combination antiretroviral therapy (cART)-resistant HIV strains may have contributed to more aggressive forms of HIV encephalitis (HIVE). However, since not all patients with HIVE display neurodegeneration and motor-cognitive impairment, it is possible that, in some cases, the host is capable of producing trophic factors that protect neuronal, glial, and endothelial cell populations from HIV-associated toxicity. Identification of new trophic factors, and improved understanding of neuroprotective mechanisms, may lead to new treatments for HIVE in the cART era.

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