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Home | Pregnancy Timeline | News Alerts |News Archive Aug 5, 2013

 

Expression levels of many of the 50 mutation-containing genes that may form
a 'schizophrenic' bias, tested highest early in fetal development; tapered off
by childhood, but again conspicuously increased in early adulthood –
just when schizophrenia symptoms typically are first observed.





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Prenatal gene network suspected in schizophrenia

A prenatal gene may disrupt the birth of new neurons in the developing prefrontal cortex.

Researchers have reverse-engineered the outlines of a disrupted prenatal gene network in schizophrenia, by tracing spontaneous mutations to where and when they likely cause damage in the brain. Some people with the brain disorder may suffer from impaired birth of new neurons, neurogenesis, in the front of their brain during prenatal development, suggests the study, which was funded by the National Institutes of Health.

"Processes critical for the brain's development can be revealed by the mutations that disrupt them," explained Mary-Claire King, Ph.D., University of Washington (UW), Seattle, a grantee of the NIH's National Institute of Mental Health (NIMH). "Mutations can lead to loss of integrity of a whole pathway, not just of a single gene. Our results implicate networked genes underlying a pathway responsible for orchestrating neurogenesis in the prefrontal cortex in schizophrenia."

King, and collaborators at UW and seven other research centers participated in the NIMH genetics report published August 1, 2013 in the journal Cell.

"By linking genomic findings to functional measures, this approach gives us additional insight into how early development differs in the brain of someone who will eventually manifest the symptoms of psychosis," said NIMH Director Thomas R. Insel, M.D.

Earlier studies have linked spontaneous mutations to non-inherited schizophrenia and traced them to genes involved in brain development, but little was known about other effects ocurring along neural pathways. King and colleagues set out to explore causes of schizophrenia by researching resources that show where in the brain and when in development genes turn on. They then compared spontaneous mutations in 105 people diagnosed with schizophrenia, to mutations in 84 unaffected siblings in families without previous histories of the illness.

Unlike most other genes, expression levels of many of the 50 mutation-containing genes that form the suspected network, tested highest early in fetal development; tapered off by childhood, but again conspicuously increased in early adulthood – just when schizophrenia symptoms typically are first observed.

This adds to evidence supporting the prevailing neurodevelopmental model of schizophrenia. The implicated genes play important roles in cell migration in the developing brain, communication between brain cells, regulation of gene expression, and related intracellular behaviors.


Having an older father increased the likelihood of spontaneous mutations for both affected and unaffected siblings.


Yet affected siblings in the study sample had up to 21 percent of  the schizophrenia mutations predicted. Although mutations tend to be individually rare, only one gene harboring damaging mutations turned up in more than one of the cases, and several patients had damaging mutations in more than one gene.

The networks formed by genes harboring these damaging mutations were found to vary in connectivity, based on the extent to which their proteins are co-expressed and interact. The network formed by genes harboring damaging mutations in schizophrenia had significantly more nodes, or points of connection, than networks modeled from unaffected siblings. By contrast, the network of genes harboring non-damaging mutations in affected siblings had no more nodes than similar networks in unaffected siblings.


When the researchers compared network connectivity across different brain tissues during different periods of development, they discovered one notable difference between affected and unaffected siblings:

Genes harboring damaging mutations expressed in the fetal prefrontal cortex of people with schizophrenia, form a network with significantly greater connectivity than networks modeled from genes harboring similar mutations in their unaffected siblings—during the same period of development.


The study results are consistent with several lines of evidence implicating the prefrontal cortex in schizophrenia. The prefrontal cortex organizes information from other brain regions to coordinate executive functions like thinking, planning, attention span, working memory, problem-solving, and self-regulation. The findings suggest that impairments in such functions often begin before the onset of symptoms in early adulthood—when the prefrontal cortex fully matures—and appear to be early signs of the illness.

The study demonstrates how integrating genomic data and transcriptome analysis can help to pinpoint disease mechanisms and identify potential treatment targets. For example, the mutant genes in patients studied suggest the possible efficacy of using medications targeting glutamate and calcium channels, say the researchers.

"These results are striking, as they show that the genetic architecture of schizophrenia cannot be understood without an appreciation of how genes work in temporal and spatial networks during neurodevelopment," said Thomas Lehner, Ph.D., chief of the NIMH Genomics Research Branch.

Summary
Genes disrupted in schizophrenia may be revealed by de novo mutations in affected persons from otherwise healthy families. Furthermore, during normal brain development, genes are expressed in patterns specific to developmental stage and neuroanatomical structure. We identified de novo mutations in persons with schizophrenia and then mapped the responsible genes onto transcriptome profiles of normal human brain tissues from age 13 weeks gestation to adulthood. In the dorsolateral and ventrolateral prefrontal cortex during fetal development, genes harboring damaging de novo mutations in schizophrenia formed a network significantly enriched for transcriptional coexpression and protein interaction. The 50 genes in the network function in neuronal migration, synaptic transmission, signaling, transcriptional regulation, and transport. These results suggest that disruptions of fetal prefrontal cortical neurogenesis are critical to the pathophysiology of schizophrenia. These results also support the feasibility of integrating genomic and transcriptome analyses to map critical neurodevelopmental processes in time and space 

Original press release:http://www.eurekalert.org/pub_releases/2013-08/niom-spg073013.php