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“The human genome is providing a powerful new way in to this disease.Understanding these genetic effects on risk is a way of prying open that black box, peering inside and starting to see actual biological mechanisms.”“This study marks a crucial turning point in the fight against mental illness,” said Bruce Cuthbert, acting director of the National Institute of Mental Health.
It has now been shown to also play a key role in brain development and schizophrenia risk.
The insight may allow future therapeutic strategies to be directed at the disorder’s roots, rather than just its symptoms. 27 in , was led by HMS researchers at the Broad Institute’s Stanley Center for Psychiatric Research and Boston Children’s.
“Because the molecular origins of psychiatric diseases are little-understood, efforts by pharmaceutical companies to pursue new therapeutics are few and far between. Thanks to this genetic breakthrough we can finally see the potential for clinical tests, early detection, new treatments and even prevention.”The path to discovery The discovery involved the collection of DNA from more than 100,000 people, detailed analysis of complex genetic variation in more than 65,000 human genomes, development of an innovative analytical strategy, examination of postmortem brain samples from hundreds of people and the use of animal models to show that a protein from the immune system also plays a previously unsuspected role in the brain.
Over the past five years, Stanley Center geneticists and collaborators around the world collected more than 100,000 human DNA samples from 30 different countries to locate regions of the human genome harboring genetic variants that increase the risk of schizophrenia.
People with schizophrenia tend to think and act differently than other people because the occurrence of hallucinations, delusions and other symptoms characteristic of schizophrenia causes them to experience reality very differently than other people.
The risk of schizophrenia increases if a person inherits specific variants in a gene related to “synaptic pruning”—the elimination of connections between neurons—according to a study from Harvard Medical School, the Broad Institute and Boston Children’s Hospital.
Stevens, a recent recipient of a Mac Arthur Foundation “genius grant,” had found that other complement proteins in the immune system also played a role in brain development.
These results came from studying an experimental model of synaptic pruning in the mouse visual system.
The strongest signal by far was on chromosome 6, in a region of DNA long associated with infectious disease.
This caused some observers to suggest that schizophrenia might be triggered by an infectious agent.