The rescue, described as “surprisingly complete” by the researchers, was carried out with rapamycin, a drug known to act on a protein called mTOR, whose role involves the production of other proteins. The idea of testing the effectiveness of this drug to save the loss of nerve cells occurred to the team because he had discovered a new gene that appears to act in concert with two previously identified susceptibility genes for schizophrenia, such as are involved in the activation of mTOR. The assembly of multiple genes adds support for the idea that susceptibility to schizophrenia and autism may have common DNA, the researchers said.This study was supported by the National Institutes of Health, the McKnight Foundation, NARSAD, the International Organization for Mental Health Research, the research fund stem cell Maryland, and the March of Dimes.
Johns Hopkins report using a drug available on the market successfully to “save” the brain cells of animals that were intentionally damaged by manipulating a gene recently discovered that the susceptibility genes for schizophrenia and autism links.
The new neurons with alterations of DISC1, KIAA1212 or AKT in the brains of mice treated with rapamycin developed normally, says Hongjun Song, Ph.D., associate professor of neurology at the Institute for Cell Engineering at Johns Hopkins Medicine, who co- research. “What was surprising for us is how the drug works, at least at the cellular level,” he said. “A number of defects in neural development – the size of the cell extended cellular localization of the error and abnormal neuronal processes involved in receiving and sending messages – were corrected by this single drug.”
Cell Engineering at Johns Hopkins University School of Medicine. “The next step is to create a good animal model that would allow us to verify whether the candidate drug to reverse not only the irregularities of brain cells to a deficiency of these genes, but as behavior.”
Since mTOR is a downstream effector AKT known, adult mice treated with rapamycin accommodate these abnormal neurons, a drug known to reduce the effects of a defective AKT path. It ‘actually “saved” neurons of their defects.
Found the gene, called KIAA1212, serves as a bridge between two genes in schizophrenia: DISC1 and AKT. Suspecting KIAA1212 as one of many potential binding partners interact with DISC1, whose name stands for “Trouble in schizophrenia,” the researchers genetically closed the production of DISC1 protein in neurons of the hippocampus region of the newborn in the adult mouse brain . The hippocampus contains a niche in which stem cells give rise to fully developed the newborn neurons. The idea was to deliberately cause these cells to malfunction and then look what happened.
In a report on the work published on September 24 issue of the journal Neuron, the researchers are careful to say that the genes in question are not the cause of schizophrenia or other brain / mind disorder in humans. However, these genes appear to be a model for the proteins that constantly arise in a variety of mental illnesses in people.
The authors on the paper, in addition to Ming and Song, are Ju Young Kim, Xin Duan, Cindy Y. Liu, Jang Mi-Hyeon, Junjie U. Guo, Nattapol Pow-anpongkul Eunchai and Kang, all of Johns Hopkins.
Scientists have discovered that new neurons were significantly worse 14 days after deletion DISC1 were defective in a variety of ways. By manipulating AKT production, or altering KIAA1212, found the same abnormalities that with DISC1 deficiency, concluding that KIAA1212 is in the same signaling pathway as DISC1 and AKT.