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Tomorrow's Antidepressants
According to NIMH-funded scientists, new research adds to evidence of potentially better molecular targets in the brain to treat depression and other mental disorders.
The researchers suggest that imbalances in the activity of an enzyme called GSK3B may be closer to the root cause of mental illnesses than are low serotonin levels. Serotonin, a brain chemical, is the ultimate target of several current medications that work by indirectly increasing it to relieve symptoms. In preliminary findings, the scientists suggest that GSK3B might be a more fundamental--and thus, perhaps, better and faster--target for new medications.
In the new study, even when serotonin levels stayed low, the scientists were able to correct abnormal, mental-illness-like behaviors in mice by blocking GSK3B. When activated, GSK3B plays a crucial role inside brain cells by sending chemical signals that help regulate cell function--but this activity must occur at the right time and in the right amount for the brain to function properly.
About Serotonin
Serotonin is one of several neurotransmitters through which brain cells communicate with each other. Abnormalties in the serotonin system are known to occur in depression, bipolar disorder, anxiety disorder, autism, and schizophrenia, for example.
However, abnormalities in the serotonin system increasingly seem to be just one part of chains of molecular events that underlie various mental disorders. Recent research reveals that components such as GSK3B are involved in these chains of events.
In this study, scientists based their experiments on a gene that makes Tph2, another enzyme involved in serotonin production. A variation of that gene has been linked to depression in some people, and in this study, mice genetically engineered with an equivalent mutation in the Tph2 gene had an 80 percent drop in brain serotonin levels.
As serotonin levels dropped, the GSK3B enzyme went into action, sending chemical signals into brain cells, and the mice developed abnormal behaviors. The scientists corrected the abnormal behaviors not by increasing serotonin levels, as current medications for many mental disorders do, but by blocking the GSK3B enzyme, instead.
Taken together, the results offer evidence that both the GSK3B enzyme and the Tph2 gene play a role in some mental disorders.
Source: National Institute of Mental Health
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