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Simon provides a clear and well-focused discussion on the question, “What causes infarction in ischemic brain?” Recently, attention has turned to a central feature of ischemic brain injury, acidosis. Targeting this effector of injury as a therapy for brain injury, he cites, may now be closer at hand and may result in robust neuroprotection.
Lewis and Moghaddam point out that impairments in certain cognitive functions mediated by dorsolateral prefrontal cortex, such as working memory, are core features of schizophrenia. Convergent findings suggest that these disturbances are associated with alterations in markers of both inhibitory γ-aminobutyric acid and excitatory glutamate neurotransmission in dorsolateral prefrontal cortex. They review the evidence that these findings suggest specific targets for therapeutic interventions to improve cognitive function in patients with this neurological disorder.
This Month in Archives of Neurology. Arch Neurol. 2006;63(10):1364–1365. doi:10.1001/archneur.63.10.1364
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