This is an announcement of no small importance that appeared on the Columbia University website. The researchers say they have reversed one of the most important symptoms of schizophrenia in mice by reversing the SETD1A gene mutation, a gene already known and previously linked by other studies to schizophrenia. Specifically, the researchers reversed the impairment of spatial working memory.
For schizophrenia, there are currently no real treatments. This pathology, which influences the functioning of the brain as well as behavior and mood, must be linked to a sort of cognitive impairment. However, the drugs that exist today for schizophrenia mostly control the psychotic symptoms and not the cognitive ones. This new study shows that it is possible, in a sense, to repair brain cells made dysfunctional by schizophrenia, at least in mice, bringing their level of working memory back to a pre-existing state.
The study, published in Neuron, therefore shows what Joseph Gogos, a researcher at Columbia’s Brain Behavior Institute and senior author of the study, defines as a “promising path” to treat schizophrenia, particularly damage to working memory, not always treated with antipsychotic drugs. An inoperative working memory makes it difficult to maintain any kind of relationship and even damages everyday life by literally putting on by people with schizophrenia who can no longer interact with other people.
The researchers worked on the SETD1A gene. The latter produces a protein that can influence the activity of other important genes. The researchers worked on a group of memory-deficient mice, mice that had some difficulty, for example, in moving into a simple maze. These mice presented neurons from the different prefrontal cortex of normal mice. Specifically, mice lacking SETD1A had short and poorly developed neuronal branches.
This prevented them from establishing the necessary connections with other groups of brain neurons, as Jun Mukai, the study’s first author and former researcher in the Gogos laboratory, explains. By manipulating the SETD1A gene they discovered that it was linked to another gene, called LSD1. By inhibiting the latter, the memory of the mice greatly improved so that their axons began to grow again, becoming similar to those of healthy mice.
Researchers say SETD1A influences a number of other genes and proteins that, combined, can cause memory deficits. This finding could be useful, according to the researchers, to make personalized drugs for people with SETD1A gene mutations and, in a broader view, even to treat schizophrenia itself.
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