For this week, I had a bit of a difficult time finding an article through the library database, so I turned to other ways of finding articles. I used backtracking to find a really interesting article that relates directly to my research question and might be able to help me better develop my proposal. The article is call “An epigenetic mechanism links socioeconomic status to changes in depression-related brain functions in high-risk adolescents” by J. R. Swartz, A. R. Hariri, and D. E. Williamson. The article investigates the biological factors behind the development of mental illness and how life stressors can trigger them more readily in certain people, depending on their situation. Specifically, it previously had been found that increased risk for developing a mental illness due to life stressors can be triggered through methylation of gene regulatory regions, which results in epigenetic modification of gene expression. With this information in mind, the authors asked “is differential gene methylation a function of adversity that contributes to the emergence of individual risk for mental illness?”. They used the neuroimaging and behavioral data of 132 adolescents. It was found that lower socioeconomic status during childhood is related to an increase in methylation of the serotonin transporter gene. This causes the amygdala to be more sensitive and exhibit more threat-related activity, which increases risk for depression. It was also found that there is an association between increases in this type of activity from the amygdala due to life stressors and having a family history of depression. The article states that “these initial results suggest a specific biological mechanism through which adversity contributes to altered brain function, which in turn moderates the emergence of general liability as individual risk for mental illness.”.
Swartz, J. R., Hariri, A. R., Williamson, D. E. (2017). An Epigenetic Mechanism Links Socioeconomic Status to Changes in Depression-Related Brain Function in High-Risk Adolescents. Molecular Psychiatry. (Vol. 22, pp. 209-214.)