Experimental drugs are showing promise against neuroAIDS, the nerve damage caused by HIV infection that lessens many patients' ability to think and move. As evidence of the progress, researchers at the University of Rochester Medical Center today received a $7 million grant to confirm that two new drug classes can protect the brain from HIV-related nerve damage. Driving their approach is the realization that antiviral drugs that work against AIDS do not cure neuroAIDS.
As many as 900,000 Americans are infected with the human immunodeficiency virus (HIV), which attacks immune cells and leaves patients vulnerable to infection. Before the arrival of modern antiviral therapies in 1996, HIV also had a devastating effect on the brain known as HIV-associated dementia (HAD) or neuroAIDs. The current, standard combination of treatments has extended the lives of most U.S. AIDS patients, but has not cured neuroAIDS, despite early reports to the contrary. Antiviral combinations only slow the onset of HIV-related nerve damage that is becoming more common the longer HIV patients live.
Where patients suffered rapid, severe neurological damage before combination therapy, they now gradually lose attention span, memory, speaking ability and decision-making skills despite the best available treatment. The realization that anti-viral drugs do not cure HAD led researchers to ask whether there is something else about HIV besides its attack on immune cells that causes disease in the brain. The emerging answer is that the indirect effects of infection, like proteins released by the virus and chemicals released by human cells reacting to them, are toxic in themselves.
As a result, labs nationwide are urgently searching for compounds that counter such toxins, with several now in human trials. These include antioxidant medications, calcium channel antagonists, NMDA antagonists like the Alzheimer's drug Memantine, platelet activating factor (PAF) inhibitors, and i
Contact: Greg Williams
University of Rochester Medical Center