Genetic Variant in Patients with Schizophrenia and Manic-depressive Disorder Impairs Communication within Brain

May 4, 2009

A genetic mutation that is commonly seen in individuals with schizophrenia and manic-depressive disorder actually plays only a minor role in such disorders and is present among �healthy� people, new research has found.

A genetic mutation that is commonly seen in individuals with schizophrenia and manic-depressive disorder actually plays only a minor role in such disorders and is present among “healthy” people, new research has found.

Scientists from the Zentralinstitut für Seelische Gesundheit in Mannheim, Heidelberg University and Bonn University in Germany conducted the current study as a follow-up to findings published a year ago that showed that a mutation in ZNF804A (rs1344706) was responsible for an increased risk of schizophrenia.

The previous research was conducted on individuals already affected by schizophrenia or manic-depressive disorder. The new study, done only with healthy participants, found that those with the ZNF804A mutation “exhibited a change in the communication between their dorsolateral prefrontal cortex (DLPFC) and other regions of their brains.” Additionally, individuals with the gene mutation showed an increased connection between the amygdala and other regions of the brain, “which is why we have related this phenomenon to the bipolar impairment, which is, as we know, characterised by erratic mood swings,” said Professor Dr. Henrik Walter of Bonn University.

In a finding to the contrary, the researchers also discovered that “the link between the DLPFC and the hippocampus was improved.” Past research showed the same results in patients already affected by schizophrenia.

Dr. Christine Esslinger of the Zentralinstitut für Seelische Gesundheit reminded carriers of the gene that the mutation “plays only a minor role in these disorders" and that those with the mutation should remember that a large amount of other factors are involved in their development.

The function of a protein in the mutated gene has not been fully understood yet. However, the researchers are hopeful that this discovery will aid in the approach of new treatment development.

Findings of the study were published in the journal Science

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