Mouse study paves way for more effective antidepressant

Depression affects the well-being of a significant number of adults in the United States. Although medication is available for treating clinical depression, some of these drugs take a long time to work or may pose health risks because of their side effects. However, a new mouse study paves the way for a more effective treatment of depression in humans.
A new mouse study finds an innovative avenue for developing more effective antidepressant medication.

The Centers for Disease Control and Prevention (CDC) report that 8 million U.S. individuals were diagnosed with major depressive disorder between 2009 and 2010, and that the condition accounted for almost 43,000 deaths during that time.

Treatment options available for people with depression include psychotherapy and medication. Antidepressants work for most people, however for others, the side effects pose serious health risks. The medication may lead to suicidal thoughts or even suicide attempts in some people, especially during the initial period of 2 to 4 weeks before the drugs start to work.

In an attempt to come up with a better alternative to the antidepressants currently on the market, researchers from the University of California (UC) San Diego School of Medicine have set out to study depression in mice. The team – led by Abraham Palmer, Ph.D., professor of psychiatry and vice chair for basic research at the UC San Diego School of Medicine – found that inhibiting a certain enzyme alleviates symptoms of depression in mice.

The findings were published in the journal Molecular Psychiatry.

Glyoxalase 1 inhibitor relieved depression-like symptoms in mice

Palmer and team inhibited an enzyme called Glyoxalase 1 (GLO1). GLO1 has been shown to inhibit, in its turn, a byproduct that results from the cell’s metabolism. This byproduct inhibits neurons and influences mood and behavior.

Previous research has shown that increased GLO1 can raise anxiety in mice, but the new study adds…

Read the full article from the Source…

Leave a Reply

Your email address will not be published. Required fields are marked *