Brain Chemical Finding Could Open Door to New Schizophrenia Drugs

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New research has linked psychosis with an abnormal relationship between two signalling chemicals in the brain. The findings, published in tomorrow’s edition of the journal Biological Psychiatry, suggest a new approach to preventing psychotic symptoms, which could lead to better drugs for schizophrenia.

Schizophrenia is one of the most common severe mental health conditions. Sufferers experience symptoms of psychosis — an inability to distinguish between reality and imagination — such as hallucinations and delusions. The condition tends to begin in the late teens or twenties, and usually persists for the rest of the sufferer’s life.

Brain chemicals called neurotransmitters carry signals from one nerve cell to another. Research has linked schizophrenia with abnormally high levels of a neurotransmitter called dopamine in a region of the brain called the striatum. Drugs currently used to treat schizophrenia block the effects of dopamine in the brain. These drugs are not effective for all patients, and can have serious side effects.

The new pilot research, funded by the Medical Research Council (MRC), provides evidence that high levels of dopamine in people with psychotic symptoms occur as a consequence of changes in another brain chemical, glutamate. Glutamate-releasing cells in a brain region called the hippocampus connect to the striatum and influence the activity of dopamine-releasing cells. Drugs that interfere with glutamate signals in the brain might therefore be able to prevent psychotic symptoms in people with schizophrenia…..

Reported by ScienceDaily
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Imperial College London, via EurekAlert!, a service of AAAS.
http://www.sciencedaily.com/releases/2010/09/100930101543.htm

Journal Reference: Stone. Altered Relationship Between Hippocampal Glutamate Levels and Striatal Dopamine Function in Subjects at Ultra High Risk of Psychosis. Biological Psychiatry, 2010; 68 (7): 599 DOI: 10.1016/j.biopsych.2010.05.034

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