old man
Picture for representation Pixabay

A drug currently in development for the treatment of Leukemia can potentially cure Schizophrenia as it managed to reverse in adult mice a previously untreatable symptom of the impairment of spatial working memory.

Researchers at the University of Columbia hope to have found a way to treat schizophrenia-associated working memory deficits as the team used a mouse model to successfully reverse a mutation in the gene SETD1A, which has previously been associated with the disorder.

The research published in Neuron said mutations to this particular gene conferred a large "increase" in risk for Schizophrenia – a neuropsychiatric disorder extremely difficult to understand, let alone the treatment.

To this day, there is no standard treatment for working memory impairment which is a core feature of Schizophrenia with symptoms such as an effect on the patient's mood, behaviour, and the ability to function.

Schizophrenia's most well-known symptoms including paranoia, auditory hallucination, and delusion are often controlled with antipsychotic medication, but disruption to working memory largely remains untreatable.

"We were surprised to see that restoration of SETD1A activity in the brain of adult mice restored their learning," explained neuroscientist Joseph Gogos from Columbia's Zuckerman Institute.

Gogos said that the results were a promising step towards the use of knowledge from genetic studies to "identify drugs that restore normal cognitive and cellular function in the adult brain" after the onset of Schizophrenia.

The research found that switching another gene LSD1 off disappeared the harmful effects of SETD1A, meaning that repurposing the LSD1 inhibitor drug improved the animals' memory "within a few weeks of administering an LSD1 inhibitor".

Neuroscientist Jun Mukai said axons in the brain of mice "grew in similar patterns to what we see in a healthy mouse brain".

Gogos concluded that his team hoped to infer how these mutations affected the development and function of the human brain by analyzing how they affected the mouse brains.