Synaptic pruning may sound like a landscaping technique at first glance, but, in fact, it is a process our brains go through during early childhood and adolescence where weak connections between neurons are destroyed. Generally, this is to make room for newer, stronger bonds that can incorporate the new information we have learned or new reasoning techniques. During the teen years, the brain loses about half of the connectors in the Prefrontal Cortex, where our brains make decisions and evaluate the risks a person should and should not take.
For the last decade, there has been a theory in neuropsychological circles that this process of synaptic pruning impacts the development and progression of psychosis-based disorders, such as schizophrenia and bipolar disorder. In a recent study1 published this week in Nature and conducted by Harvard University, this hypothesis has further cemented. By reviewing the genetic data from 65,000 individuals, researchers have been able to conclude that the presence of the C4 gene, which causes excess synaptic pruning, is more prevalent in those with schizophrenia and can indicate a higher risk of the development of the disease.
While this study focuses on only one disease, this does open up more discussion for other psychiatric diseases that have psychosis as a component of their symptoms. Symptoms of psychosis include delusions, hallucinations, and impaired ability to analyze and express thoughts and emotions. These diseases have previously only been diagnosed through the Diagnostic Statistical Manual (DSM) criteria based solely on behaviors that are observed or reported by the patient and those around him. Symptoms are usually first seen in the young adult years and progress in severity over the patient’s lifetime. However, the average time from onset to diagnosis is typically ten years, leaving the disease unchecked to ravage the minds and lives of the patient in the interim.
This new knowledge of the connection between the C4 gene and schizophrenia can lead to a quick diagnosis with genetic screenings and earlier treatment of the disease. Additionally, this can lead to medications that may attack the disease early on at it’s root cause rather than managing the symptoms of psychosis and mood instability. While this is being touted as the first study solidly linking physiological information and genetic indicators to psychiatric disease development, there was in fact prior evidence of persistent psychosis associated with infantile autism linked to the synaptic pruning of the Medial Frontal Lobe2 and reduced neuroplasticity and brain volume in psychotic adolescents3. Both of these previous studies indicate that synaptic pruning can be further generalized to most, if not all, psychosis-based disorders.
1Sekar, A. et al. (2016). Schizophrenia risk from complex variation of complement component 4. Nature. Retrieved February 3, 2016, from http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16549.html
2 Saugstad, L. (2011). Infantile autism: A chronic psychosis since infancy due to synaptic pruning of the supplementary motor area. Nutrition and Health,20(3-4), 171-182. Retrieved February 3, 2016, from http://www.ncbi.nlm.nih.gov/pubmed/22141191
3 Rapoport, J. L., & Gogtay, N. (2008). Brain Neuroplasticity in Healthy, Hyperactive and Psychotic Children: Insights from Neuroimaging. Neuropsychopharmacology, (33), 181-197. Retrieved February 3, 2016, from http://www.nature.com/npp/journal/v33/n1/abs/1301553a.html