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Genetic trigger of depression identified: Potential target for novel class of therapeutic agents

Date:
October 18, 2010
Source:
Yale University
Summary:
Researchers have found a gene that seems to be a key contributor to the onset of depression and is a promising target for a new class of antidepressants.

A called MKP-1 seems to be a key contributor to the onset of depression and is a promising target for a new class of antidepressants.
Credit: iStockphoto/Dieter Hawlan

Yale University researchers have found a gene that seems to be a key contributor to the onset of depression and is a promising target for a new class of antidepressants, they report Oct. 17 in the journal Nature Medicine.

"This could be a primary cause, or at least a major contributing factor, to the signaling abnormalities that lead to depression," said Ronald S. Duman, professor of psychiatry and pharmacology at Yale and senior author of the study.

Scientists have had a difficult time pinning down the cause of depression, which afflicts almost 16 percent of Americans in any given year and carries an annual economic burden of $100 billion.

Symptoms of depression vary widely among individuals. Most now believe that multiple physiological processes are involved in major depressive disorder. That explains why people respond differently to most commonly prescribed antidepressants, which work by manipulating the uptake of the neurotransmitter serotonin. However, as many as 40 percent of depressed patients do not respond to currently available medications, which take weeks to months to produce a therapeutic response.

Duman's team did whole genome scans on tissue samples from 21 deceased individuals who had been diagnosed with depression and compared gene expression levels to those of 18 individuals who had not been diagnosed with depression. They found that one gene called MKP-1 was increased more than two-fold in the brain tissues of depressed individuals.

This was particularly exciting, say the researchers, because the gene inactivates a molecular pathway crucial to the survival and function of neurons and its impairment has been implicated in depression as well as other disorders. Duman's team also found that when the MKP-1 gene is knocked out in mice, the mice become resilient to stress. When the gene is activated, mice exhibit symptoms that mimic depression.

The finding that a negative regulator of a key neuronal signaling pathway is increased in depression also identifies MKP-1 as a potential target for a novel class of therapeutic agents, particularly for treatment resistant depression.

Other Yale authors include Vanja Duric, Mounira Banasr, Pawel Licznerski, Heath D Schmidt, Arthur A Simen and Samuel S Newton.

The work was funded by the U.S. Health Service and State of Connecticut, Connecticut Mental Health Center.


Story Source:

The above story is based on materials provided by Yale University. Note: Materials may be edited for content and length.


Journal Reference:

  1. Vanja Duric, Mounira Banasr, Pawel Licznerski, Heath D Schmidt, Craig A Stockmeier, Arthur A Simen, Samuel S Newton, Ronald S Duman. A negative regulator of MAP kinase causes depressive behavior. Nature Medicine, 2010; DOI: 10.1038/nm.2219

Cite This Page:

Yale University. "Genetic trigger of depression identified: Potential target for novel class of therapeutic agents." ScienceDaily. ScienceDaily, 18 October 2010. <www.sciencedaily.com/releases/2010/10/101017133639.htm>.
Yale University. (2010, October 18). Genetic trigger of depression identified: Potential target for novel class of therapeutic agents. ScienceDaily. Retrieved October 20, 2014 from www.sciencedaily.com/releases/2010/10/101017133639.htm
Yale University. "Genetic trigger of depression identified: Potential target for novel class of therapeutic agents." ScienceDaily. www.sciencedaily.com/releases/2010/10/101017133639.htm (accessed October 20, 2014).

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