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See Latest ArticlesGlycogen synthase kinase-3β (GSK-3β) inhibitors AR-A014418 and B6B3O prevent human immunodeficiency virus-mediated neurotoxicity in primary human neurons
Journal of Neurovirology, 08/21/09
Nguyen TB et al. – Results support the ability of glycogen synthase kinase-3β (GSK-3β) inhibition to be neuroprotective against HIV-associated neurotoxicity by reducing HIV associated procaspase induction. These data support a role for GSK-3β as a potential therapeutic target and may have important clinical implications for treatment of HIV-associated neurocognitive disorder.
Methods- Study of the specificity of 2 GSK-3β-specific inhibitors, AR-A014418 (A) and B6B30 (B) to prevent direct neurotoxicity in primary human neurons exposed to HIV (BaL)
- Investigation of acute and ongoing mechanisms of HIV neurotoxicity
- Exposure of neurons to HIV (500 pg/mL) for 12-hr and 6-day periods in presence/absence of A (1 µM, 100 nM, 10 nM) and B (50 nM, 5 nM, 500 pM)
- Lactate dehydrogenase (LDH) assay to assess cytotoxicity
- Luminescence assay to measure activity of acute proapoptotic markers caspases 3 and 7
- Significant neurotoxic effect of HIV from control values was not restored via coexposures of all concentrations of A and B
- No change in LDH levels after 6 days
- Acute proapoptotic markers caspases 3 and 7 activity increased by HIV exposure (BaL) vs controls
- Effect ameliorated via coexposure to all concentrations of A and 50 nM B after 12 hr and to all concentrations of A and B after 6 days
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