The team found that MKP-1 plays the role of an ‘off switch’ over a cascade of brain chemicals called MAPK that are crucial to the survival and function of neurons. Lead author Ronald Duman, a professor of psychiatry and pharmacology said, “This could be a primary cause [of], or at least a major contributing factor to, the signaling abnormalities that lead to depression.”
For the study the team created special mice whose MKP-1 had been deactivated to explore the hypothesis that altering MAPK levels played a role in depression. Mice without MKP-1 were resilient to stress. But stressed mice with the gene developed depression-like symptoms which were then eased by using anti-depression drugs, they found.
However authors warn that depression like many other mood disorders may be more than gene deep. 40% of patients do not respond to currently available medications and these patients might have this genetic abnormality feel researchers.
According to Douglas Meineke, program chief at the National Institute of Mental Health, “This paper contributes a new and potential target for therapies… I would describe it as an important, small piece in a slowly emerging jigsaw puzzle.” Dr. Duman said that the next step is to see if these findings can lead to a medication that can inhibit the MKP-1 gene.