14 DAY TRIAL // Scientists at the Johns Hopkins University (JHU) have just published two new studies, showing why the onset of schizophrenia may be facilitated in young adults, as opposed to older people. The investigators say that two anatomical abnormalities were identified in the brain, and the subsequent researcher proved that they might be playing a role in the onset of these mental conditions. The cortical mechanisms that promote the development of the disease are deeply rooted into these “glitches,” the experts report, quoted by e! Science News.
In one of the research papers, JHU experts show that the abnormalities are considerably influenced by the DISC1 gene. This conclusion was drawn from studies of a particular Scottish family, which has a long history of members who developed schizophrenia, as well as a hoist of related conditions. Researchers are hopeful that the new data could in the near future be used to develop new approach to either preventing or combating the symptoms associated with this mental disease. The team also says that the idea proposed by other investigators, who say that abnormal synaptic connectivity in the brain may be a promoter of this disease, has a lot of merit.
In the paper the group published – which will appear in the upcoming March issue of the esteemed scientific publication Nature Neuroscience – they show that young adulthood is a time of massive rewiring in the brain. These rearrangements of synapses, coded by the DISC1 gene in a faulty manner, could be one of the promoters of symptoms associated with schizophrenia. “Connections between neurons are constantly being made and broken throughout life, with a massive amount of broken connections, or 'pruning,' happening in adolescence. If this pruning doesn't happen correctly, it may be one reason for the pathogenesis of schizophrenia,” says JHU School of Medicine professor of psychiatry Akira Sawa, MD, PhD, who was also the leader of the study.
The second research paper, also produced by Sawa's team, and published in the February 25 issue of the journal Nature, details the creation of a new animal model for this disease. The group manipulated lab mice genetically, so that their brains stopped producing the DISC1 gene in their prefrontal cortices. The reason why this particular brain region was selected is because it is known to look different in schizophrenia patient, on brain scans. Additionally, doing so allowed the scientists to study some of the secondary effects that the gene has on the rodents' brains.
“If we can learn more about the cascade of events that lead to these anatomical differences, we may eventually be able to alter the course of schizophrenia. During adolescence, we may be able to intervene to prevent or lessen symptoms,” Sawa concludes.