Researchers at the University of Heidelberg in Germany have found that disrupting one protein (SRGAP3) in mice causes mental changes similar to those occurring in some neurological and psychological disorders in children, such as those linked to schizophrenia.
Studies of whole genomes in humans have revealed that genes implicated in intellectual disability, autism and schizophrenia overlap quite a lot, perhaps because of the roles of these genes in neural development. Specifically, these genes tend to be involved synaptic plasticity: the strengthening and weakening of connections between neurons. Previously, the gene coding for the SRGAP3 protein has been implicated in the risk of schizophrenia.
Therefore, Dr Bartsch and colleagues created genetically modified mice that had an inactive SRGAP3 protein. Without this single protein, the mice displayed several of the behavioural features seen in schizophrenia-related developmental disorders. For example, they had spontaneous tics and deficits in social interaction. The majority of mice also had enlarged lateral ventricles, which is a feature of schizophrenia. In some mice, this had developed into hydroencephalus (brain swelling due to excess fluid inside the skull), which occurs in humans from problems with neural stem cells. Since this protein plays a similar role in humans and mice, it is not unreasonable to suggest that the malfunction of SRGAP3 could be involved in these neurodevelopmental disorders.
Though nothing in genetics or neuroscience is ever simple, it seems that one protein may be heavily involved in several neurodevelopmental disorders, and understanding how it works could help provide new treatments for these disorders by dealing with the biological cause, not just the symptoms.