To: John Wright who wrote (773 ) 2/11/2000 8:06:00 AM From: Dr. John M. de Castro Read Replies (1) | Respond to of 1494
Attached is the abstract of a very nice study demonstrating one of the ways that memantine can be useful in the treatment of AIDS dementia complex. I especially like the statement "The neurotoxicity .. was blocked completely by memantine" Craig, I'll look forward to your May 15 birthday. Hopefully you'll also have an NTII present (translate partnership). The institutional buying is very significant. The stock price is finally up to a level where they can buy. Many institutions are prohibited from purchasing shares below $5. Now, just as soon as NTII pops up above the $5 level the institutions start jumping in. This suggests that there is considerable confidence on the street in the future of NTII. It also means that a large number of shares will be in steady hands, thus reducing the effective float. This should provide an even greater pop when good news is released as there will be fewer shares available for the buyers. Best regards John de C Synergistic neurotoxicity by human immunodeficiency virus proteins Tat and gp120: protection by memantine. Ann Neurol 2000 Feb;47(2):186-94 Nath A, Haughey NJ, Jones M, Anderson C, Bell JE, Geiger JD Department of Neurology, University of Kentucky, Lexington 40536-0284, USA. Human immunodeficiency virus type 1 (HIV-1) proteins Tat and gp120 have been implicated in the pathogenesis of dementia associated with HIV infection. Recently, we showed the presence of Tat protein in brains of patients with HIV-1 encephalitis as well as macaques with encephalitis caused by a chimeric strain of HIV and simian immunodeficiency virus, and that even transient exposure of cells to Tat leads to release of cytopathic cytokines. Now, we report the first demonstration of gp120 protein in brain of patients with HIV encephalitis. We tested the hypothesis that Tat and gp120 would act synergistically to potentiate each protein's neurotoxic effects and determined the extent to which pharmacological antagonists against processes implicated in HIV-1 neuropathogenesis could block HIV-1 protein-induced neurotoxicity. Subtoxic concentrations of Tat and gp120, when incubated together, caused neuronal cell death and prolonged increases in levels of intracellular calcium. A transient exposure of neurons to Tat and gp120 for seconds initiated neuronal cell death, but maximal levels of neuronal cell death were observed with exposures lasting 30 minutes. The neurotoxicity caused by Tat and gp120 applied in combination was blocked completely by memantine, partially by amiloride, and not at all by dipyridamole or vigabatrin