Fighting hidden challenges
Neurologist William Tyor developed a genetically altered mouse model of the HIV-related cognition dysfunction seen in humans.
Day 8: Atlanta Veterans Affairs Medical Center
Last spring, Emory's Veterans Program formally opened a new intensive outpatient treatment program for post-9/11 veterans, which aims to reduce symptoms of post-traumatic stress disorder, while helping veterans re-engage in daily life.
When Lamar Jenkins, 42, walked into William Tyor's office at the Atlanta Veterans Affairs Medical Center (VAMC), the neurologist already had a pretty good idea of what the man's partner was about to describe.
Fogginess, confusion, forgetting to turn off the stove. Tyor had seen it too many times before.
The number of cases of HIV-associated dementia dropped markedly with the arrival of powerful antiretroviral drugs that reduce viral load, restore immune response, and result in longer, healthier lives. But these drugs don't halt neurocognitive impairment found in 40% or more of people living with HIV. Jenkins's disorder had progressed to the point where he could no longer be left alone.
For the past 30 years, since AIDS first appeared on the scene, Tyor has investigated what causes these problems.
The partnership between Emory and the Atlanta VA Medical Center dates back to 1946. Emory provides virtually all physician care at the facility and has made it one of the nation's most successful VA centers for research to continually improve care. Emory investigators contribute to a diverse spectrum of research at the Atlanta VA that brought in more than $14 million in VA and $12.5 million in non-VA funding last year.
In the body, HIV destroys infection-fighting white blood cells and thus lowers the immune response. When the virus enters the brain, however, HIV infects micro-glial cells that fight infections in the brain, distorting the cells in a way that raises the immune response. This results in inflammation, which can destroy neurons essential to cognition and memory.
The usual antiretroviral drugs don't eradicate the virus from the brain and thus don't fight the inflammation. Different medicines are needed for that.
After developing a genetically altered mouse model of the HIV-related cognition dysfunction seen in humans, Tyor began testing numerous compounds until he found one that reduces inflammation and slows disease progression. In fact, it seemed to reverse memory problems in mice that received the compound early in the disease process, perhaps before too many neurons died.
Tyor hopes patients like Jenkins might benefit from the new compound. He and Emory colleagues are preparing for a clinical trial in humans. With the largest population of HIV/AIDS patients of any VAMC in the country, the Atlanta facility is a great research partner for this effort, and its patients will be the first to potentially benefit.