Gene biomarker may determine whether some depression drugs will work

Although treatments for depression have been shown to work rather well, researchers have been unable in the past to determine why some people respond better than others to the class of drugs that includes Prozac, Zoloft and Celexa. Now, a team at Tel Aviv University has uncovered a gene that may act as a biomarker for this type of patient, potentially helping to match the drug with the patient.

Selective serotonin reuptake inhibitors, or SSRIs, are designed to help the brain use more of the neurotransmitter serotonin by blocking its reabsorption. This helps brighten moods, according to a report from American Friends of Tel Aviv University, by rebuilding connections in the brain, but the specific process by which it works is still unknown. It is known, however, that only part of the population is responsive to the treatment.

So the researchers exposed 80 cell lines from the biobank at the National Laboratory of the Genetics of Israeli Populations, each cell line representing the genome of a potential depression patient, to the depression drug paroxetine, or Paxil, from GlaxoSmithKline ($GSK). When they compared the most responsive cell lines to the least responsive cell lines, they found that a gene called CHL1 showed lower levels in those who responded more actively to the treatment. Thus, the gene could potentially act as a biomarker for patients that will respond to SSRIs. For those who don't, another treatment option might work better.

"SSRIs only work for about 60 percent of people with depression," said researcher David Gurwitz in a statement. "A drug from other families of antidepressants could be effective for some of the others. We are working to move the treatment of depression from a trial-and-error approach to a best-fit, personalized regimen."

So instead of going through a line of drugs to reach the one that will work best, the researchers foresee a simple blood test that will rule at least some of them out. If the gene does in fact play such a role, it could change the hypothesis about how SSRIs are thought to work, which is that they act on the neurotransmitter instead of the gene. This approach could also lead to more personalized treatment for Alzheimer's disease, as well, according to the report.

- here's the American Friends of Tel Aviv University report
- read the journal article

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