Jan 082014
 

No Me Mireis! (Photo credit: El Hermano Pila)

Scientists cured mice of stress-induced depression using new drugs.

For the last century, research on depression has focused on neurons. But a new study by Israeli and American researchers shows that another type of cell, called the microglia, can cause depression in situations of prolonged stress.

What’s more, they found that using new types of drugs to stimulate the microglia enabled them to cure the depressive symptoms in mice more effectively than could be done using existing anti-depressants.

The researchers from the Hebrew University of Jerusalem and the University of Colorado plan to test the clinical effectiveness of these drugs on human patients in the near future.

The study, which was financed by the National Science Foundation, was published this week in the journal “Molecular Psychiatry.” It was conducted by Hebrew University Prof. Raz Yirmiya and doctoral student Tirzah Kreisel in conjunction with colleagues from the University of Colorado.

That prolonged stress can lead to depression is well known. But the current study, based on experiments conducted in mice, is the first to argue that microglia play a significant role in this process. Specifically, changes in the structure and functioning of microglia can cause depression in situations of prolonged stress, the researchers found.

Microglia, which constitute about 10 percent of all brain cells, are essentially the immune system’s “agents” in the brain. Like immune cells in other parts of the body, they play a role in fighting off bacteria and viruses. But they also play a unique physiological role in brain activity, including in its response to stress situations.

The study involved putting mice in daily situations of moderate but unpredictable stress.

After five weeks of this, the mice developed symptoms of depression: They displayed no interest in pleasurable activity like social play or drinking sweetened beverages, and their production of new brain cells decreased.

Read more . . .

via Haaretz (Free Registration Required)
 

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