Abstract
Several evidences support the hypothesis that glutamatergic dysfunction may be implicated in the pathogenesis of schizophrenia and in the last few years great interest has been focused on the role of the N-methyl-D-aspartate receptor (NMDAR). Glutamate is the main excitatory neurotransmitter in human CNS and it plays a prominent role in synaptic plasticity, learning, and memory and other cognitive functions. Increasing interest in memantine add-on therapy in schizophrenic patients with negative and cognitive symptoms may suggest that memantine could be a new promising treatment in schizophrenia. The aim of this update was to evaluate clinical data about the memantine effectiveness in schizophrenic patients. Our systematic review of the literature highlights that memantine therapy in schizophrenic patients seems to improve mainly negative symptoms while positive symptoms and cognitive symptoms did not improve significantly.
Highlights
Schizophrenia is a chronic illness characterized by positive symptoms and negative symptoms that leads to progressive functional and cognitive impairment.The aetiology of schizophrenia is not well determined, but alterations and disturbances of developmental processes have been hypothesized by many researchers [1, 2].For many years, a glutamatergic dysfunction has been implicated in the pathogenesis of schizophrenia [3] and recently great interest has been focused on the role of the Nmethyl-D-aspartate receptor (NMDAR) [4, 5]
A glutamatergic dysfunction has been implicated in the pathogenesis of schizophrenia [3] and recently great interest has been focused on the role of the Nmethyl-D-aspartate receptor (NMDAR) [4, 5]
These substances bind the intrachannel site of the receptor and prevent calcium ion flux into the cell, leading to effects that mimic those seen in schizophrenia including hallucinations, delusions, thought disorder, and, most notably, negative symptoms [16,17,18]
Summary
Schizophrenia is a chronic illness characterized by positive symptoms and negative symptoms (such as reduction of emotional responsiveness, motivation, socialization, speech, and movement) that leads to progressive functional and cognitive impairment.The aetiology of schizophrenia is not well determined, but alterations and disturbances of developmental processes have been hypothesized by many researchers [1, 2].For many years, a glutamatergic dysfunction has been implicated in the pathogenesis of schizophrenia [3] and recently great interest has been focused on the role of the Nmethyl-D-aspartate receptor (NMDAR) [4, 5]. The link between glutamate, NMDAR, Journal of Amino Acids and schizophrenia was firstly suggested by psychotomimetic symptoms induced by NMDAR noncompetitive antagonists, such as ketamine and phencyclidine, in healthy subjects [16]. These substances bind the intrachannel site of the receptor and prevent calcium ion flux into the cell, leading to effects that mimic those seen in schizophrenia including hallucinations, delusions, thought disorder, and, most notably, negative symptoms [16,17,18]. We could say that memantine can recognize and block pathologically activated NMDARs whereas it does not influence the normal functioning of physiologically activated receptors, and this property is not shared by ketamine and PCP: this could be the reason why ketamine, PCP, and memantine are all NMDARs antagonist, they show so different effects
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