Researchers at Columbia University's Zuckerman Institute report promising advancements in tackling memory loss, a hallmark symptom of schizophrenia.
Schizophrenia affects over 23 million people worldwide, according to the World Health Organization (WHO). This severe, chronic mental disorder involves distortions in thinking, behavior, emotions, and sense of self, often manifesting as hallucinations, delusions, and false beliefs. A 2015 study confirmed its genetic roots.
Published in the journal Neuron on October 9, 2019, new research targets memory loss—a persistent symptom despite treatments like medication and psychosocial support. The team posits that inhibiting a specific gene offers a path to restoration.
Memory deficits in schizophrenia stem from mutations in the SETD1A gene, which produces a protein that regulates other genes. These mutations occur years before symptoms emerge. In lab mice engineered to produce less SETD1A protein, schizophrenia-like behaviors appeared.
Direct manipulation of SETD1A remains challenging, but scientists identified its interaction with the LSD1 gene. Inhibiting LSD1 neutralized SETD1A's harmful effects. After weeks of LSD1 inhibitor treatment in mice, memory improved markedly, linked to healthier axons—the neuron extensions that transmit electrical signals to synapses.
These findings illuminate SETD1A's role and open doors to novel, personalized treatments. While not a cure, they pave the way for targeted therapies.
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