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- W2048531806 abstract "Work from our laboratories has validated mixed lineage kinase type 3 (MLK3) as an enzyme pathologically activated in the CNS by human immunodeficiency virus 1 (HIV-1) neurotoxins. In this review, we discuss MLK3 activation in the context of the neuropathogenesis of HIV-1 associated neurocognitive deficits (HAND). We use findings from the literature to substantiate the neuropathologic relevance of MLK3 to neurodegenerative disease, with an emphasis on Parkinson’s disease that shares a number of important phenotypic and neuropathologic characteristics with HAND. We discuss signal transduction pathways downstream from MLK3 activation, with an emphasis on their involvement in microglia and neurons in preclinical models of HAND. Finally, we make a case for pharmacologic intervention targeted at inhibition of MLK3 as a strategy to reverse HAND, in light of the fact that combination antiretroviral therapy, despite successfully managing systemic infection of HIV-1, has been largely unsuccessful in eradicating HAND." @default.
- W2048531806 created "2016-06-24" @default.
- W2048531806 creator A5009468541 @default.
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- W2048531806 creator A5076244533 @default.
- W2048531806 creator A5079760958 @default.
- W2048531806 date "2010-10-01" @default.
- W2048531806 modified "2023-09-27" @default.
- W2048531806 title "Rebuilding synaptic architecture in HIV-1 associated neurocognitive disease: A therapeutic strategy based on modulation of mixed lineage kinase" @default.
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- W2048531806 doi "https://doi.org/10.1016/j.nurt.2010.08.001" @default.
- W2048531806 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2948545" @default.
- W2048531806 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20880503" @default.
- W2048531806 hasPublicationYear "2010" @default.