Dr. Gurwitz believes that among our 25,000 human genes, only a few hundred will show a difference between the two types of "extreme responder" cells. In the next phase of their study, they will explore which of those "hits" can be valuable clinical biomarkers for the response to Prozac, a study that can subsequently be done by psychiatrists.

"Ours is a unique model because it does not make presumptions," says Dr. Gurwitz. "Research on Prozac response biomarkers over the past 20 years has focused on genes related to the brain metabolism of serotonin, long suspected as the cause of depression," he adds. "However, after many years of research with this focus, it is now obvious that the approach has failed. We realize that we must look at the entire repertoire of human genes."

"Psychiatric pharmacology remains a black box," says Dr. Gurwitz. "Nobody knows why some people respond to Prozac-type SSRI anti-depressants, while others are helped by other kinds of antidepressants. The World Health Organization predicts by the year 2020, costs and lost productivity from depression will exceed those of cardiovascular disease as the leading cause of health expenditure in developed countries. We hope to produce a clear test for antidepressant drug responses to improve the odds for successful treatment."

Source: American Friends of Tel Aviv University