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Clinical

Protein kinase CK2: A new class of antidepressant treatment coming?

Staff Writer
Staff Writer 6 years ago
Updated 2019/06/28 at 7:39 PM
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Today, for those suffering from affective disorders, selective serotonin reuptake inhibitors (SSRIs), the most popular class of antidepressants, are commonly prescribed to diminish symptoms.

A recent study, however, has found that altering a protein named casein kinase 2 (CK2) may treat symptoms of depression and anxiety as well, possibly leading researchers to a new class of antidepressants. As published in Molecular Psychiatry, researchers at City College of New York examined the role of CK2 and its association with 5-HT4, a serotonin receptor.

According to Julia Castello, one of the lead researchers, manipulating CK2 in the brain causes an inhibition of affective symptoms, such as depression and anxiety. CK2’s beneficiary effects work by modulating the 5-HT4 receptor, researchers say.

“Our findings identify the mPFC as the region that mediates the effect of enhanced 5-HT4 receptor activity and CK2 as modulator of 5-HT4 receptor levels in this brain region that regulates mood-related phenotypes,” the study reads.

The investigation into CK2 could result in the formation of new antidepressants and increase our current understanding of serotonin receptors and mood disorders.

“Identifying new targets broadens our understanding about the cause of depression as well as the mechanism of action of antidepressants, which could lead to the formulation of new antidepressants that work more efficiently and faster for more people,” Castello stated.

In prior research, CK2 has been investigated for its possible role in Parkinson’s, a neurodegenerative disease. The protein also contributes to the modulation of L-DOPA induced dyskinesia, the findings concluded.

More research on CK2’s effectiveness for mood-related disorders to be expected, researchers suggested.

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TAGGED: 5-HT4 receptor, antidepressants, anxiety, CK2, depression, L-DOPA, protein, serotonin receptor
Staff Writer January 22, 2018
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