Public release date: 8-Dec-2009

 

 

English: The compound is an inhibitor of monoa...

 

TORONTO, Dec. 8 /CNW/ – A key brain protein called monoamine oxidase A (MAO-A) – is highly elevated during clinical depression yet is unaffected by treatment with commonly used antidepressants, according to an important study published today in the Archives of General Psychiatry. The study has important implications for our understanding of why antidepressants don’t always work.

 

Researchers at the Centre for Addiction and Mental Health (CAMH) used an advanced brain imaging method to measure levels of the brain protein MAO-A. MAO-A digests multiple brain chemicals, including serotonin, that help maintain healthy mood. High MAO-A levels excessively remove these brain chemicals.

 

 

Antidepressant medications are the most commonly prescribed treatments in North America, yet 50 per cent of people do not respond adequately to antidepressant treatment. Dr. Jeffrey Meyer the lead investigator explains, “Mismatches between treatment and disease are important for understanding why treatments don’t always work. Rather than reversing the problem of MAO-A breaking down several chemicals, most antidepressants only raise serotonin.”

 

 

Understanding the Problem of a Persistent Illness

 

 

Depression ranks as the fourth leading cause of disability and premature death worldwide, according to the World Health Organization. Recurrent illness is a major problem. Even under the most optimal treatment circumstances, recurrence rates for clinical depression are at least 20 per cent over two years.

 

 

The new study also focused upon people who had fully recovered from past episodes of clinical depression. Some people who appeared to be in recovery actually had high levels of MAO-A. Those with high levels of MAO-A then had subsequent recurrence of their depressive episodes.

 

 

This new idea of high levels of MAO-A lowering brain chemicals (called monoamines), then falling into a clinical depression is consistent with the historical finding that medications which artificially lower monoamines can lead to clinical depression as a side effect. In the 1950’s some medications to treat high blood pressure also lowered monoamines and people began to experience depressive episodes. When the medications were removed, people recovered.

 

 

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