The finding is the first in humans to show that a receptor, which is pivotal to the action of widely prescribed anti-anxiety medications, may be abnormal in the disorder and help to explain how genes might influence vulnerability.
In the study, positron emission tomography (PET) determined that three brain areas of panic disorder patients are lacking in a key component of a chemical messenger system that regulates emotion, says Alexander Neumeister, MD, of the National Institute of Mental Health (NIMH). Brain scans revealed that the component, a type of serotonin receptor, is reduced by nearly a third in three structures straddling the center of the brain, according to the report in the current issue of The Journal of Neuroscience.
“This is first time anyone has shown, in vivo, a decrease in serotonin binding in panic disorder patients. Eventually, this work could lead to new more selective pharmacological treatments that would specifically target this receptor,” says Michael Davis, PhD, of Emory University, who studies anxiety disorders. “Clinical studies like this are extremely important for guiding basic research in animals to understand more fully the role of these receptors in anxiety.”
Each year, panic attacks strike about 2.4 million American adults “out of the blue,” with feelings of intense fear and physical symptoms sometimes confused with a heart attack. Unchecked, the disorder often sets in motion a debilitating psychological sequel syndrome of agoraphobia, avoiding public places. Panic disorder runs in families and researchers have long suspected a genetic component.
In the study, Neumeister and his colleagues used PET scans to visualize serotonin 5-HT1A receptors in the brains of 16 panic disorder patients – seven of whom also suffered from major depression – and 15 matched healthy controls. In the panic disorder patients, including those who also had depression, receptors were reduced by an average of nearly a third in the anterior cingulate in the front middle part of the brain, the posterior cingulate, in the rear middle part of the brain, and in the raphe, in the midbrain.
Unfortunately it doesn't sound like these researchers had the genes for 5-HT1A sequenced in this group of patients. Though even if they had it is possible that such a test wouldn't find the genetic difference causing this difference in receptor concentration. The genetic difference may be at a different site in the genome that codes for a regulatory protein or a piece of regulatory RNA (interference RNA) that regulates this gene. this group of patients do not
Because the disorder can run in families, experts have suspected that certain genetic variations might make people more vulnerable to developing it. The new research gives weight to that idea.
"This is the first study that shows a very clear biological difference in patients and controls," Neumeister said.
The illness, which most commonly begins between late adolescence and the mid-30's, is just one in a group of anxiety-inducing ailments that are relatively widespread. About 19 million Americans are afflicted by one of the diseases; obsessive-compulsive disorder, post-traumatic stress disorder and specific phobias are among the more well known.
It is interesting to note that a genetic variation of the 5-HT1A receptor gene is correlated with depression. Differences in the same receptor have been found to also correlate with differences in beliefs about spirituality.
|Share |||Randall Parker, 2004 February 26 09:53 AM Biological Mind|