How the SETD1A gene produces schizophrenia in mice
A new study published in the journal Neuron on October 9, 2019 reports that scientists have unlocked part of the secrets of the SETD1A gene – how mutations in the gene put the individual at risk for the condition.
The researchers inactivated this gene, which they call “a master regulator”, in a mouse model, producing loss of working memory, just as in patients with schizophrenia. On the other hand, restoring the function of the gene brought the working memory back to normal function. In addition, reversal of this inactivation in adult mice also led to improvement of the affected neuronal circuits. This shows that it may be possible to treat patients with schizophrenia due to SETD1A abnormality.
Researcher David Panchision says, “This schizophrenia risk gene codes for an enzyme that influences the expression of many other genes. In mice, a hobbled version of SETD1A disrupted gene expression in a network harboring other genomic suspects in schizophrenia. Remarkably, the resulting abnormalities were reversible.”
The SETD1A gene
The SETD1A gene is among the few that may be definitely associated with schizophrenia. It has been found to exist in several forms, some of which are rare while others are common. However, all of these increase the risk of schizophrenia, making SETD1A mutations one of the few genetic factors that are assuredly known to put the individual at risk for this psychosis. There are a host of other genetic changes that are more common in schizophrenia, but they contribute small individual effects to the risk. However, having just one abnormal SETD1A gene increases the schizophrenia risk markedly.
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