How Brain Cell ‘Switches’ Might Trigger Schizophrenia Symptoms

What is it about?

This article proposes a new explanation for how certain brain functions may go wrong in people experiencing psychosis or schizophrenia. It suggests that specific brain cell 'switches' — called potassium channels and HCN (hyperpolarization-activated cyclic nucleotide-gated) channels — may not be working properly in the prefrontal cortex (the brain’s control center for decision-making and thinking) and possibly in other brain regions. When these 'switches' don’t close correctly, it can disrupt how brain cells communicate. This disruption may contribute to symptoms such as: hallucinations; disorganized thinking; impaired judgment; inability to feel pleasure; loss of motivation; problems with memory and concentration.

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Photo by Hal Gatewood on Unsplash

Photo by Hal Gatewood on Unsplash

Why is it important?

Current treatments are not always able to treat schizophrenia symptoms like: hallucinations, disorganized thinking, impaired judgment. Delirium psychosis involves similar symptoms and is consistently resistant to current treatments. This article's theory proposes another explanation and possible solution for these challenging symptoms. It also addresses the overlooked schizophrenia symptoms such as: the inability to feel pleasure, low motivation, and cognitive difficulties. These symptoms are consistently resistant to current treatments, which helps explain why in the European Union where healthcare is widely accessible, 80%-90% of patients with schizophrenia remain unemployed and 10% die by suicide. Targeting and closing these 'switches' could be especially beneficial for these overlooked symptoms. This article also matters because it can improve our general understanding of schizophrenia and psychosis. The current theory suggests that having too much dopamine (a chemical messenger in the body that controls movement, among other functions) causes these disorders. However, this does not explain why certain drugs that lower dopamine can produce schizophrenia symptoms, or why dopamine-increasing substances such as nicotine can improve certain symptoms. Modulation of these 'switches' can explain these discrepancies. The dopamine theory is not wrong, but it is incomplete. Understanding this may lead to innovative treatments and shed light on why the new schizophrenia drug iclepertin failed, why potassium channel opening drugs are unlikely to succeed, and how the new drug Cobenfy may perform. In short, this article challenges the idea that schizophrenia and psychosis are only about dopamine, and instead points to a more complete understanding that could guide future treatments.

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