Scientists Discover Schizophrenia Gene Roles in Brain Development

Posted on June 12, 2018

A research team identified 150 proteins affecting cell activity and brain development that contribute to mental disorders. It is the first time these molecules, which are associated with the disrupted-in-schizophrenia 1 (DISC1) protein linked to mental disorders, have been identified. The scientists developed new tools involving stem cells to determine chemical reactions the proteins use to influence cell functions and nerve growth in people.

Schizophrenia affects less than 1 percent of the U.S. population, but has an outsized impact on disability, suicide and premature deaths. The DISC1 gene was linked to schizophrenia nearly 20 years ago. It controls how nerve cells called neurons develop, as well as how the brain matures. DISC1 also directs a network of signals across cells that can contribute to the disease. Scientists say errors in these chemical reactions contribute to schizophrenia.

However, the identity of proteins that DISC1 can regulate is poorly understood, prompting the researchers to undertake the research. Using stem cells, they conducted assays resembling habitat where DISC1 does its work. Then, they used gene editing to insert a molecular tag on DISC1, allowing them to extract it from brain cells and identify the proteins with which it associates. Identifying the proteins that interact with DISC1 in brain cells could lead to understanding how the risk factors for psychiatric diseases are connected to specific molecular functions. The discovery enables researchers to determine specific processes that differ in patients suffering from specific mental illnesses.

Schizophrenia is one of the top 15 leading causes of disability worldwide. People with schizophrenia live an average of nearly 29 years less than those without the disorder. With this research, researchers now have specific trails to follow within cells from both healthy patients and those diagnosed with disorders.


Category(s):Schizophrenia

Source material from Science Daily


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