NIH Researchers Identify Pathway that May Protect Against Cocaine Addiction
A study by researchers at NIH gives insight into changes in the reward circuitry of the brain that may provide resistance against cocaine addiction. Scientists found that strengthening signaling along a neural pathway that runs through the nucleus accumbens—a region of the brain involved in motivation, pleasure and addiction—can reduce cocaine-seeking behavior in mice.
Research suggests that about 1 in 5 people who use cocaine will become addicted, but it remains unclear why certain people are more vulnerable to drug addiction than others.
“A key step in understanding addiction and advancing treatment is to identify the differences in brain connectivity between subjects who compulsively take cocaine and those who do not,” said Dr. Ken Warren, acting director of the National Institute on Alcohol Abuse and Alcoholism. Researchers at NIAAA conducted the study.
“Until now, most efforts have focused on finding traits associated with vulnerability to develop compulsive cocaine use. However, identifying mechanisms that promote resilience may prove to have more therapeutic value,” said the paper’s senior author, Dr. Veronica Alvarez, acting chief of the section on neuronal structure in NIAAA’s Laboratory for Integrative Neuroscience. The study appeared in Nature Neuroscience.
Anti-HIV Therapy Appears to Protect Children’s Hearts, NIH Study Shows
|For children who have had HIV-1 infection since birth, the combination drug therapies now used to treat HIV appear to protect against the heart damage seen before combination therapies were available.
For children who have had HIV-1 infection since birth, the combination drug therapies now used to treat HIV appear to protect against the heart damage seen before combination therapies were available, according to researchers in an NIH network study.
In the early 1990s, children with HIV were not treated with anti-HIV therapy or were treated with only one drug. In recent years, children, like adults, have been treated with combinations of three or more anti-HIV medications. This combination approach is called highly active antiretroviral therapy, or HAART.
Before the widespread use of HAART, many children with HIV had chronic heart disease. In fact, heart failure was the underlying cause of death for 25 percent of HIV-infected children who died after age 10. However, doctors knew little about whether combination anti-HIV drug therapies could affect the heart. In this study, researchers examined heart structure and function of more than 500 children born to HIV-infected mothers. They then compared the data with results from an NHLBI-sponsored study of HIV-infected children, conducted in the 1990s.
“NIH has been committed to investigating the effects of HIV and its treatment on the heart,” said study co-author Dr. Rohan Hazra of the Maternal and Pediatric Infectious Disease Branch, NICHD, one of 10 NIH institutes or offices that supported the study. “Our study indicates that anti-HIV medication may protect the heart.”
The findings appeared online in JAMA Pediatrics.
Suppressing Protein May Stem Alzheimer’s Disease Process
Scientists funded by NIH have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer’s disease. It’s based on unclogging removal of toxic debris that accumulates in patients’ brains, by blocking activity of a little-known regulator protein called CD33.
“Too much CD33 activity appears to promote late-onset Alzheimer’s by preventing support cells from clearing out toxic plaques, key risk factors for the disease,” explained Dr. Rudolph Tanzi of Massachusetts General Hospital and Harvard University. “Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.”
Tanzi and colleagues reported their findings Apr. 25 in the journal Neuron.
“These results reveal a previously unknown, potentially powerful mechanism for protecting neurons from damaging toxicity and inflammation,” said NIMH director Dr. Thomas Insel. “Given increasing evidence of overlap between brain disorders at the molecular level, understanding such workings in Alzheimer’s disease may also provide insights into other mental disorders.”
Variation in the CD33 gene turned up as one of four prime suspects in the largest genome-wide dragnet of Alzheimer’s-affected families, reported by Tanzi and colleagues in 2008. The gene was known to make a protein that regulates the immune system, but its function in the brain remained elusive. To discover how it might contribute to Alzheimer’s, the researchers brought to bear human genetics, biochemistry and human brain tissue, mouse and cell-based experiments.