Kamal SM and Dine SE
Neuroplasticity is pointed to the ability of the brain to change its molecular and structural characteristics that hinder its function. The main pathophysiological alteration in schizophrenic patients is the occurrence of a major deficit in cognitive process that is under the control of the circuitry of the dorsolateral prefrontal cortex (DLPFC) [1,2]. Additionally, this cognitive deficit in schizophrenia is partially related to the marked decrease in dopamine [DA] input to the DLPFC. However and fortunately, a compensatory response in the form of up-regulation of D1 receptor in this area of brain results in a great improvement of memory-related DLPFC activity.
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