Neuroplasticity in Treatment of Schizophrenia

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). Additionally, this cognitive deficit inschizophrenia 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.

Studies performed by Elvevag, Goldberg  and Black assumed that schizophrenic patients suffered from brain atrophy, neurotoxicity, or neurodegeneration that involved loss of neurons in the gray matter. Additionally, the reduction in brain volume was due to shrinkage of the neuropil surrounding the neurons with marked reduction in dendrite length that was associated with a reduction in the number and size of dendritic extensions.

This disorder is related to an alteration in the functional activity of the dorsolateral prefrontal cortex (DLPFC). DLPFC is a brain region that is related to thecontrol of executive function. Any abnormalities in the function of DLPFC are strongly related to the development and progress of schizophrenic symptoms.