Bing:
According to an article on Medical Xpress, researchers at Rutgers and Emory University have found that mitochondrial dysregulation is a contributor to the development of schizophrenia¹. The study focused on the strongest-known genetic risk factor for schizophrenia, a small portion of chromosome 3 that is missing, known as 3q29 deletion syndrome¹. This deletion increases the risk for schizophrenia by about 40-fold¹.
The researchers analyzed overlapping patterns of altered gene activity in two models of 3q29 deletion syndrome, including mice where the deletion has been engineered in using CRISPR, and human brain organoids, or three-dimensional tissue cultures used to study disease¹. Both systems exhibited impaired mitochondrial function, which can cause energy shortfalls in the brain and result in psychiatric symptoms and disorders¹.
Jennifer Mulle, an associate professor at Rutgers Robert Wood Johnson Medical School and a co-senior author of the study, said that their data give strong support to the hypothesis that mitochondrial dysregulation is a contributor to the development of schizophrenia¹. The findings converge with work on another genetic risk factor for schizophrenia, 22q11 deletion syndrome (or DiGeorge syndrome), which has also been found to involve disrupted mitochondrial function¹.