Schizophrenia risk gene linked to cognitive deficits in mice ▫️Researchers have discovered in mice how one of the few genes definitively linked to schizophrenia, called SETD1A, likely confers risk for the illness. - Mice genetically engineered to lack a functioning version of the enzyme-coding gene showed abnormalities in working memory, mimicking those commonly seen in schizophrenia patients. Restoring the gene's function corrected the working memory deficit. - Counteracting the gene's deficiencies also repaired neuronal circuit deficits in adult mice - suggesting clues for potential treatment strategies. ▫️Researchers have identified both common and rare genetic variations that contribute to risk for schizophrenia. Mutant SETD1A is one of just a few rare genes known to unequivocally confer risk for schizophrenia. - While common genetic variations linked to schizophrenia individually exert only tiny effects on risk, having just one mutant copy of SETD1A is sufficient to confer a large increase in disease risk. ▫️SETD1A plays a key role in epigenomic regulation - the switching on-and-off of genes in response to experience - a molecular process widespread in the brain. - Mutations in SETD1A have primarily been found in people with schizophrenia, suggesting that this rare gene variation might hold important clues to the underlying disease process. ▫️Reactivating SETD1A function or counteracting downstream effects of SETD1A deficiency in the adult brain, perhaps with LSD1 inhibitors, may hold promise for treating schizophrenia's cognitive deficits, suggest the researchers.
