Genetic scientists believe that a possible cause of schizophrenia could be reversed, eliminating symptoms of the disorder. The study focuses on Neuregulin(NRG1), a protein that plays an important role in synapses, and the development and identification of different cells in the nervous system, known as gene coding. Multiple studies have NRG1 as a fundamental contributor in the development of schizophrenia and associated symptoms. In mice, when these levels were elevated, much like human patients, the mice began to demonstrate similar symptoms that we attribute to the disorder. By lowering the protein, or blocking it, the researchers eliminated those different behavioral patterns.
Current treatments have come a long way, and many can lead relatively normal and fulfilling lives, but most medications are targeting different neurotransmitters at an attempt to lower the effects but can’t cure the disease. If this protein is creating the severity of behaviors, then possible treatments could prevent humans at risk or suffering from progressing into the disorder, and reverse those who may already be experiencing the result.
No one cause is linked directly to schizophrenia, however, many genetic markers drastically increase the risk of developing it. Schizophrenia tends to run in families, and many environmental triggers can increase potential risks. It is undeniably important that more comprehensive treatments are found. At this time, anti-psychotic medications are the most important treatment, and additional support and coping tools can be implemented in order to help decrease effects of both negative and positive symptoms. Strong support and access to appropriate medical care can mean the difference between suffering with the disorder, or living with it. New medical technology and therapies could have the potential to be life-changing, and those with known gene linkages could potentially be treated before symptoms even arise. The next step is to see if we can recreate the success in subjects other than mice.
By: Courtney Kidd, LMSW
SJS Staff Writer
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