MONDAY, May 9, 2005 (HealthDay News) -- New research suggests a variation on one gene can disrupt a mental circuit, making people more susceptible to depression and anxiety.
The circuit controls the body's ability to silence a ringing alarm in the brain when a human feels fear, said study co-author Dr. Daniel R. Weinberger, director of the Genes, Cognition and Psychosis Program at the National Institute of Mental Health. Brain scans showed that people with less effective circuitry were more likely to have trouble dealing with the stresses of life, he added.
The findings won't immediately lead to new treatments for mental illness, Weinberger noted. In fact, antidepressants already target some related circuitry in the brain.
However, he said the research gives scientists more understanding into how people cope -- and don't cope -- with the slings and arrows of life.
"We're chipping away at what previously seemed like such complex human qualities," he said.
In previous studies, Weinberger and other researchers examined a gene that helps to program the brain's system to deal with the chemical serotonin. Lack of the neurotransmitter contributes to depression, and common antidepressants make it easier for the brain to keep serotonin levels steady.
The researchers found evidence that one of the two types of the gene -- the "short" type -- contributes to general anxiety and the risk of depression following major life stresses. It also heightens the brain's response to viewing scary faces.
In the new study, Weinberger and colleagues examined the brain scans of 114 healthy people to see the effect of having one or two copies of the short type of the gene. Humans come with two copies of the gene, inherited from their parents. Each copy is "long" or "short."
The researchers found that those with at least one short copy of the gene had less effective circuitry in the part of the brain that controls responses to fear. That meant they had less gray matter, fewer neurons and fewer neural connections.
The findings appear in the May 8 online issue of Nature Neuroscience.
"The problem is not the alarm clock, but the button you push to stop the alarm," which doesn't work correctly in those people, Weinberger said.
Researchers linked the effectiveness of the circuit to the subjects' vulnerability to depression and anxiety. That makes sense, Weinberger said, because in affected people "the problem isn't that you're fearful, it's that you can't stop being fearful, you can't turn it off."
But the genetic variation doesn't by itself guarantee that someone will become depressed or anxious, Weinberger said. Other factors -- both environmental and genetic -- contribute to helping a person develop depression or anxiety, he said.
Dr. James Grisolia, a neurologist at Scripps Mercy Hospital in San Diego, said the study findings will need to be confirmed. But for now, the potential link between gene variations and brain changes "underscores that tiny changes in the DNA code have the potential to cause far-reaching changes in the person."
In another depression-related study released this month, American and German researchers armed with brain scans found evidence that depression doesn't affect the level of pain felt by patients with fibromyalgia, a condition that causes chronic pain. The findings appear in the May issue of Arthritis & Rheumatism.
More information
To learn more about depression, visit the National Institute of Mental Health.
