The organoids grown from patients and controls differed in their expression of thousands of genes – in line with the finding that the genetic influences on schizophrenia are many and very small. However, among the genes, those associated with neuronal axons stood out as a group.
Importantly, the researchers assessed organoid maturation at several time points, which enabled them to establish the persistent nature of the disturbances throughout development. CYFIP1 is highly expressed in microglia, the brain’s own immune cells, but its function there is unknown. Microglia are known to carry out synaptic pruning, in which they “eat” excess synaptic structures, a process critical to healthy brain development.
Dr. Perlis said of the work, “Our findings suggest that changes in the behavior and function of microglia due to aberrant CYFIP1 function, such as through coding or copy number variants, could affect microglial processes such as synaptic pruning, homeostatic surveillance, and neuronal maintenance, which are critical for proper brain development and function. This could contribute to CYFIP1-related neurodevelopmental and psychiatric disorders resulting in part from microglia dysfunction.
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