Release date: 2009-09-22
In a groundbreaking study published in the online edition of Nature Medicine, researchers discovered that a unique variant of a potassium channel found 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 developing more effective treatments for this complex mental disorder.
Neuronal firing patterns are essential for normal brain function, but in individuals with schizophrenia, these patterns become disrupted. Scientists led by Daniel Weinberger identified a specific potassium channel called KCNH2, which is present in long-lived animals and influences how neurons fire. The hippocampus, a key region involved in memory and cognition, was found to express higher levels of KCNH2 in patients diagnosed with schizophrenia compared to healthy controls.
In a comprehensive genetic analysis involving 367 families, 1,158 unrelated cases, and 1,704 control subjects, the research team uncovered a single nucleotide polymorphism (SNP) linked to schizophrenia within the KCNH2 gene. This genetic variation was associated with lower intelligence, slower cognitive processing, and impaired memory. Additionally, individuals carrying this variant showed increased levels of hippocampal mRNA, suggesting a potential mechanism behind the disorder's development.
The study revealed that overexpression of the KCNH2 variant can lead to abnormal potassium flow in neurons, causing excessive and persistent neuronal activity. This disruption may contribute to the neurological symptoms observed in schizophrenia patients. These findings highlight the importance of ion channels in brain function and offer promising insights into future therapeutic strategies.
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