TUESDAY, June 28 (HealthDay News) -- Some HIV patients experience memory loss and other neurological deficits, despite treatment, and new research suggests that the reason why is because the virus weakens the blood-brain barrier by infecting a small group of supporting brain cells called astrocytes.
The blood-brain barrier is a network of blood vessels that protects the brain from harmful chemicals and toxins. In healthy people, astrocytes help bolster the blood vessels that comprise the blood-brain barrier.
The finding, published in the June 29 issue of the Journal of Neuroscience, may help explain why 40 percent to 60 percent of HIV patients on antiretroviral therapy experience mild to moderate neurological problems such as learning difficulties.
For this study, the researchers built a model of the blood-brain barrier using human cells in the laboratory. The research was supported by the U.S. National Institute of Mental Health.
"Our results suggest HIV infection of astrocytes may be important in the onset of cognitive impairment in people living with the disease," study author Eliseo Eugenin, of Albert Einstein College of Medicine, said in a news release from the Society for Neuroscience.
"New therapies are needed that not only target the virus, but also to stop the virus from spreading damage to other uninfected brain cells," Eugenin added.
"Researchers have been stymied to explain why HIV-associated neurological complications persist, despite potent combination antiviral therapies that have dramatically improved health and survival," Igor Grant, an expert in HIV-associated neurocognitive impairment at the University of California, San Diego, said in the news release.
"This study provides a possible explanation indicating that minute numbers of infected astrocytes can trigger a cascade of signals that could open the brain to various toxic influences," explained Grant, who was not involved with the study.
The American Psychiatric Association has more about mental health and HIV/AIDS.
SOURCE: Society for Neuroscience, news release, June 28, 2011
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