Tiny molecule can help treat mental disorders

Last Updated: Friday, June 20, 2014 - 16:35

London: The badly needed anti-depressants could be a few steps away as researchers have identified a molecule that acts on the serotonin-producing nerve cells.

It is the brain's serotonin system, which, when misregulated, is involved in depression and anxiety disorders.

The existing anti-depressants are not good enough as they do not work for around 70 percent of patients.

The Weizmann Institute's professor Alon Chen and his colleagues researched the role of microRNA molecules in the nerve cells that produce serotonin.

They succeeded in identifying, for the first time, the unique "fingerprints" of a microRNA molecule that acts on the serotonin-producing nerve cells.

Combining bioinformatics methods with experiments, the researchers found a connection between this particular microRNA (miR135) and two proteins that play a key role in serotonin production and regulation of its activities.

"These findings suggest that miR135 could be a useful therapeutic molecule - both as a blood test for depression and related disorders, and as a target whose levels might be raised in patients," said Chen.

The scientists noted that in the area of the brain containing the serotonin-producing nerve cells, miR135 levels increased when anti-depressant compounds were introduced.

"The brain needs proper miR135 levels - low enough to enable a healthy stress response and high enough to avoid depression or anxiety disorders and to respond to serotonin-boosting antidepressants," explained the researchers.

When this idea was tested on human blood samples, the researchers found that subjects who suffered from depression had unusually low miR135 levels in their blood.

On closer inspection, the scientists discovered that the three genes involved in producing miR135 are located in areas of the genome that are known to be associated with risk factors for bipolar mood disorders.

The findings appeared in the journal Neuron.

IANS

First Published: Friday, June 20, 2014 - 16:35

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