Calcium signaling dysfunction in schizophrenia: a unifying approach.
The present paper demonstrates a remarkable pervasiveness of underlying Ca(2+) signaling motifs among the available biochemical findings in schizophrenic patients and among the major molecular hypotheses of this disease. In addition, the paper reviews the findings suggesting that Ca(2+) is capable of inducing structural and cognitive deficits seen in schizophrenia. The evidence of the ability of antipsychotic drugs to affect Ca(2+) signaling is also presented. Based on these data, it is proposed that altered Ca(2+) signaling may constitute the central unifying molecular pathology in schizophrenia. According to this hypothesis schizophrenia can result from alterations in multiple proteins and other molecules as long as these alterations lead to abnormalities in certain key aspects of intracellular Ca(2+) signaling cascades.
D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology / Q000627:therapeutic use; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008959:Models, Neurological; D009419:Nerve Tissue Proteins / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism; D012559:Schizophrenia / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*
D014150:Antipsychotic Agents; D009419:Nerve Tissue Proteins; D018377:Neurotransmitter Agents; D002118:Calcium