Release date: 2009-09-22
A groundbreaking study published in the online edition of Nature-Medical has revealed that a unique variant of a potassium channel in primates plays a significant role in brain function, cognition, and neuronal activity, potentially increasing the risk of schizophrenia. This discovery opens up new possibilities for the treatment of this complex mental disorder. Properly coordinated neuronal firing is essential for normal brain function, but in individuals with schizophrenia, this process is often disrupted. Researchers led by Daniel Weinberger identified a specific potassium channel called KCNH2, which is found in long-lived animals and influences how neurons fire. The hippocampus, a key region involved in memory and learning, was central to their investigation. Comparative studies showed that KCNH2 is expressed differently in the brains of schizophrenia patients compared to healthy controls. In a large-scale analysis involving 367 families, 1,158 unrelated cases, and 1,704 control subjects, the team discovered a single nucleotide polymorphism linked to schizophrenia within the KCNH2 gene. These genetic variations are associated with lower IQ, slower cognitive processing, impaired memory, and increased levels of hippocampal mRNA. The researchers also found that overexpression of the KCNH2 variant caused an imbalance in potassium flow, leading to excessive and persistent neuronal activity, which may help explain some of the neurological abnormalities seen in schizophrenia. This research marks an important step forward in understanding the biological basis of the condition and could pave the way for more targeted therapies. Meditech Medical Network
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