Your imaginary friend, schizophrenia

Someone born in an urban environment has a fifty percent higher chance of developing schizophrenia.

“Everyone should know this stuff” Level

Schizophrenia is a disorder that has an incidence rate of 1 out of every 100 people in the world and generally surfaces in the late teens to early twenties (Bridger 2016). Some of the symptoms that are associated with schizophrenia include hallucinations, paranoia, and diminished thought processes (Bridger 2016).

Currently there is no cure for schizophrenia, so the only option is the administration of drugs that can target symptoms—most commonly psychosis (Bridger 2016). One major problem with the medications is that they do not address negative cognitive symptoms of schizophrenia (Bridger 2016). Treatment options have been limited due to a lack of understanding of the biological mechanisms as well as schizophrenia’s inability to be replicated or mimicked in cell or animal models (Stone 2016).

The use of the human genome has opened doors for researchers that were previously closed (Stone 2016). It is common knowledge in the field of psychology that schizophrenia results from a combination of biological, or genetic, factors as well as environmental influences; however, the size of the role that each of these components play is has not been definitively determined (Schizophrenia 2010b). The strong genetic component of schizophrenia means that family history plays an integral role in the calculation of the likelihood of the condition showing up in offspring (Schizophrenia 2010b). Although significant steps were made with the identification of many more genes associated with schizophrenia, this does not tell us anything if we do not also know the environmental factors responsible for turning them on (Schizophrenia 2010b).

There are four main categories of environmental factors expected to increase the risk of developing schizophrenia: place and time of birth, infections, prenatal care, and obstetrics (Schizophrenia 2010b). As shown in figure one, a child born during the winter months has a ten percent higher than average chance of developing schizophrenia (Schizophrenia 2010b). Additionally, someone born in an urban environment has a fifty percent higher chance of developing schizophrenia (Schizophrenia 2010b). All of the categories mentioned on the chart represent an increased relative associated risk for developing schizophrenia (Schizophrenia 2010b).

“For geniuses only” Level

Recently a genome-wide association study (GWAS) was carried out by researchers from the Broad Institute at Massachusetts General Hospital (MGH) in order to evaluate upwards of 80,000 genetic samples from volunteers with and without schizophrenia (Bridger 2016). This study was essential in pinpointing 108 specific locations associated with schizophrenia on the human genome—83 more than previously found (Bridger 2016). Identifying a significantly higher number of genes associated with schizophrenia has allowed researchers to recognize an established pattern in these genes, their relationships, and their functions in the brain (Bridger 2016).

Schizophrenia researchers have shown that the genes to focus on are those that are affecting neuronal and synaptic function; for example, genes that affect synaptic plasticity and more specifically postsynaptic activity (Bridger 2016). This study was recently published in the journal Nature, and was shown to locate a specific gene and its subsequent biological process as the central risk factor for the condition (Stone 2016). This new information is paving the way for the exploration of new methods of early diagnosis, treatments, or even the eventual prevention of schizophrenia altogether (Broad Institute 2016).

Initially, researchers only knew that they should be investigating chromosome 6, but soon they identified the unusual complement component 4 (C4) as the affected gene (Broad Institute 2016). C4 has a high level of structural flexibility, which means that it is common for different people to possess differing amount of copies as well as alternate types of the gene (Broad Institute 2016). Because C4 is present at the synapse, it is crucial that its levels remain controlled (Stone 2016). This is because an increase in the presence of C4 can lead to a drop in the quantity of synaptic connections, which has been linked to schizophrenia in humans (Stone 2016). With heightened C4 activity, fewer connections will be made at the synapse during the developmental stage (Broad Institute 2016).

It has also been identified that the malefactor behind schizophrenia is an abnormal variation in the major histocompatibility complex (MHC), which is a set of proteins on the surface of cells that bind to foreign molecules and presents them to the immune system (Stone 2016). It was found that this specific MHC variation directly affects the C4 gene by increasing its expression (Stone 2016). Schizophrenia researchers also found that people who possessed a certain structure of the C4 gene had an increased expression of it in their brains, and these individuals were at a heightened risk of developing schizophrenia (Broad Institute 2016). Thanks to research such as this, therapeutics can now be developed with an exact target and function in mind: the level of connections at the synapse (Broad Institute 2016).

Impress your friends and family with these three related facts:

Fact 1: Schizophrenia develops regardless of racial, ethnic, or economic background (SRDAA 2014).

Fact 2: Between one third and one half of homeless adults have schizophrenia (SRDAA 2014).

Fact 3: Treatment and other economic costs of schizophrenia are estimated between 32.5 and 65 billion dollars annually (SRDAA 2014).

Author: This page was created by Brie Bigham, a senior at Choate Rosemary Hall in Wallingford, CT. Brie’s spirit animal is the mouse. Someday, Brie will be famous for conducting a study that brings to light the major benefits of regularly watching Netflix.

 

 

 

 

Works Cited

Broad Institute of MIT and Harvard. (2016). Genetic study provides first ever insight into biological origin of schizophrenia. Science Daily. 27 January 2016. http://www.sciencedaily.com/releases/2016/01/160127141400.htm

Bridger, H. (2016). International team sheds new light on the biology underlying schizophrenia. Broad Institute. 1 February 2016. https://www.broadinstitute.org/news/5895

Public Library of Science. (2005). Comparison of a Selected Set of Relatively Well-Established Risk Factors for Schizophrenia, Focusing Mainly on Pre-and Antenatal Factors. Schizophrenia.com. 2005. http://www.schizophrenia.com/hypo.php

Schizophrenia.com. (2010a). Schizophrenia Facts and Statistics. Schizophrenia.com. 22 February 2016. http://schizophrenia.com/szfacts.htm

Schizophrenia.com. (2010b). The causes of Schizophrenia. Schizophrenia.com. 3 February 2016. http://schizophrenia.com/hypo.php

SRDAA. (2014). About Schizophrenia: DSM-5 Schizophrenia Spectrum Disorder. Schizophrenia and Related Disorders Alliance of America. http://www.sardaa.org/resources/about- schizophrenia/

Stone, M. (2016). Scientists have finally found a biological process behind schizophrenia. Gizmodo. 27 January 2016. http://gizmodo.com/scientists-have-finally-found-a-biological-process-behi-1755516643

Wilson, C. (2016). Postpartum and Straight Jackets. The Huffington Post. 26 Jauuary 2016. http://www.huffingtonpost.com/chelsey-wilson/postpartum-and-straight-j_1_b_9065884.html