Scientists at the U.S. Department of Energy’s Brookhaven National Laboratory have discovered a key mechanism in the brains of people with human immunodeficiency virus (HIV) dementia.
The study is the first to document decreases in the neurotransmitter dopamine in those with the condition, and may lead to new, more effective therapies. HIV dementia is a type of cognitive decline that is more common in the later stages of HIV infection.
“Our results offer the first evidence of dopamine terminal injury — specifically injury to dopamine transporters — in HIV dementia patients,” says Brookhaven physician Gene-Jack Wang, the study’s lead author. “This suggests that a decrease in transporters may contribute to the disease process. We believe our findings also indicate a new direction for treatment.” The study appears in the September 2004 issue of the British scientific journal Brain. Physician Linda Chang, formerly a researcher at Brookhaven Lab and now with the University of Hawaii, initiated this research.
“This study clearly demonstrates that HIV infection damages dopamine-associated brain cells, and provides a pathway for developing more effective treatments,” says National Institute on Drug Abuse (NIDA) Director Nora Volkow, co-investigator, who worked on the study while at Brookhaven Lab.
Using positron emission tomography (PET), a brain-scanning technique, Wang and colleagues looked at the brains of 15 HIV-positive study volunteers, some of whom had symptoms of dementia, and 13 HIV-negative volunteers. The purpose of the scans was to determine the presence of dopamine transporters and dopamine receptors.
Dopamine transporters, found on the terminals of some brain cells (neurons), recycle dopamine, a brain chemical that sends signals between the cells. Dopamine receptors are “docking ports” on the receiving neurons. Dopamine is associated with pleasure and reward and is also essential for movement; low levels are found in conditions such as Parkinson’s disease. Decreased dopamine transporters represent neuron damage and lower levels of functional dopamine neurons, as well as decreases in the release of dopamine.