Abstract
Clinical background Analysis of postmortem brains of patients with schizophrenia from the Stanley Foundation brain collection have shown consistent reduction of reelin, parvalbumin and GAD67, the 67-kilodalton isoform of glutamic acid decarboxylase, in the prefrontal cortex (PFC) and other brain regions [1]. In the PFC, this suggests a decrease in GABAergic inhibition that might be responsible for psychosis. Cognitive deficits are also a core symptom of schizophrenia, which might also be caused by GABAergic dysregulation.
Highlights
Analysis of postmortem brains of patients with schizophrenia from the Stanley Foundation brain collection have shown consistent reduction of reelin, parvalbumin and GAD67, the 67-kilodalton isoform of glutamic acid decarboxylase, in the prefrontal cortex (PFC) and other brain regions [1]
In the PFC, this suggests a decrease in GABAergic inhibition that might be responsible for psychosis
Cognitive deficits are a core symptom of schizophrenia, which might be caused by GABAergic dysregulation
Summary
Analysis of postmortem brains of patients with schizophrenia from the Stanley Foundation brain collection have shown consistent reduction of reelin, parvalbumin and GAD67, the 67-kilodalton isoform of glutamic acid decarboxylase, in the prefrontal cortex (PFC) and other brain regions [1]. Of Information & Communication Science, Sophia University, Tokyo 102-8554, Japan Email: Shoji Tanaka - shoji.tanaka@gmail.com from Seventeenth Annual Computational Neuroscience Meeting: CNS*2008 Portland, OR, USA. Published: 11 July 2008 BMC Neuroscience 2008, 9(Suppl 1):P36 doi:10.1186/1471-2202-9-S1-P36
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