(Great Neck, N.Y. - May 26, 2009) — While it is known that hereditary factors enhance the risk for schizophrenia and bipolar disorder, how this occurs has remained largely obscure. Now researchers in Germany have answered the question for at least one common genetic variant.
The study was led by NARSAD Investigator Andreas Meyer-Lindenberg, M.D., director of the Zentralinstitut für Seelische Gesundheit, in Mannheim, with collaborators at Heidelberg University and the University of Bonn, and was published in the May 1 issue of the journal Science. Dr. Meyer-Lindenberg was recently awarded a NARSAD Distinguished Investigator grant in support of his research, and in 2000 received a Young Investigator grant.
MRI studies of a common genetic variant associated with an enhanced risk of schizophrenia and bipolar disorder demonstrated that variant gene incurs changes in communication within the dorsolateral prefrontal cortex (DLPFC) and between the DLPFC and other brain regions.
The DLPFC plays an active role in working memory and various other higher cerebral functions. The researchers found that in those subjects with the variant gene, communication between the two halves of the DLPFC had become impaired. By contrast, the link between the DLPFC and the hippocampus, another region of the brain important for memory, was improved. Both these phenomena were known to exist in patients with schizophrenia.
Bipolar disorder is characterized by erratic mood swings. Carriers of the high-risk gene also displayed an enhanced linkage between the amygdala and other brain regions. The amygdala plays a role in regulating emotions.
The mutated gene produces a protein whose precise function is still unclear. As researchers believe is generally the case, the German investigators state that the variant form they have described appears to play only a minor role in mental disorders and must work in concert with other factors.
(This article was adapted with permission from the University of Bonn).