Citation:
Sun, Y., Gao, Y., Tidei, J. J., Shen, M., Hoang, J. T., Wagner, D. F., & Zhao, X. (2019). Loss of MeCP2 in immature neurons leads to impaired network integration. Human molecular genetics, 28(2), 245–257.
Summary of Paper:
This study follows the movement of MeCP2-deficinet neurons in the nervous system and brain. A marker was developed for the purpose of tracing neuronal movement. Something called a dual-virus monosynaptic retrograde tracing system. Two different versions of the virus were created so that htey could be visualized. Seven days after the mice were injected with the retroviruses, their brains were sectioned horizonatlly. It was found that the new adult- born neurons were depleted in their MeCP2 levels. It was also found that those neurons without the MeCP2 gene expereinced profound long-range connectivity impairments. Both of these findings were found in the observation of specifically termed dentate gyrus starter neurons. The neurons were imaged and compared with the control neurons of the mice. It was found that structurally the MeCP2 deletion group had shorter dendrites coming off the neurons and fewer branching areas. This shows that MeCP2 gene specifically plays a huge role in developent of both neurons and the entire nervous system. As a result of their findings, the scientists developed an IGF-1 molecule for genetic therapy. This molecule helped to improve the strucutal deficits found among the impaired neurons. While the results were statistically significant in physical improvment of the neuron, the scientists were unable to detect much mechanical function improvment. This paper made a large impact in laying the groundwork for genomic therapies for Rett Syn