Just last week, we had reported about the possible outcomes of tentative depression medicines. Now a new study by experts at the Centre for Addiction and Mental Health (CAMH) shows that most antidepressants may be missing the key target of clinical depression. Apparently a chief brain protein named monoamine oxidase A (MAO-A) is highly raised during clinical depression. It seems to yet be unaffected by treatment with common antidepressants.
The study claims to offer important implications for comprehending why antidepressants may not always work. Armed with an advanced brain imaging method, the experts evaluated levels of the brain protein MAO-A. Multiple brain proteins including serotonin that aid keeping in a healthy mood are known to be digested by MAO-A. Apparently high levels of MAO-A appear to excessively eliminate these brain chemicals.
According to the World Health Organization Depression is ranked as the fourth leading cause of disability and premature death worldwide. In North America antidepressant medications are known to be the most commonly prescribed treatments. In spite of this approximately 50 per cent of people appear to not respond adequately to the 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.”
A better understanding of a persistent illness, scientists suggest could offer more insights as recurrence of illness is considered to be a major problem. The recurrence rates for depression in particular are known to be at least 20 percent over two years even if the most optimal treatments are used.
For the new study, the experts centered their attention upon individuals who claimed to have completely recovered from earlier episodes of clinical depression. Interestingly some people who seemed to be in recovery actually showed high levels of MAO-A. Subsequently recurrence of their depressive episodes was observed in those with elevated levels of MAO-A.
Scientists suggest that the new idea of augmented MAO-A levels appearing to reduce brain chemicals monoamines then leading to clinical depression is apparently consistent with the historical finding that medication that artificially lowered monoamines could have clinical depression as a side effect. Some medications in the 1950s used to treat blood pressure and also reduce monoamines appeared to have resulted in depressive episodes. Individuals claimed to have recovered when they were off medications.
The study’s deployment of advanced brain imaging technology is highlighted by VP of Research Dr. Bruce Pollock, “CAMH has the only positron emission tomography (PET) centre in the world that is dedicated solely to mental health and addiction treatment and research. As a consequence, we were able to develop this new technology to measure MAO-A levels.”
While some past antidepressant medications seem to have targeted MAO-A, these inhibitors of MAO-O supposedly fell out of favor in the 1970s. This was mainly due to their adverse interactions with certain foods. Though there appear to have been improvements that overcame these problems, a wide range of antidepressant development and use seems to have overlooked the MAO-A target.
The important study has been published in the Archives of General Psychiatry.