Lidow Michael S
Department of Biomedical Sciences and Program of Neuroscience, University of Maryland, Room 5-A-12, HHH, 666 W. Baltimore Street, Baltimore, MD 21201, USA.
Brain Res Brain Res Rev. 2003 Sep;43(1):70-84. doi: 10.1016/s0165-0173(03)00203-0.
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.
本文表明，在精神分裂症患者现有的生化研究结果以及该疾病的主要分子假说中，潜在的Ca(2+)信号基序具有显著的普遍性。此外，本文回顾了一些研究结果，这些结果表明Ca(2+)能够诱发精神分裂症中出现的结构和认知缺陷。文中还介绍了抗精神病药物影响Ca(2+)信号传导能力的证据。基于这些数据，有人提出Ca(2+)信号改变可能构成精神分裂症核心的统一分子病理学。根据这一假说，只要这些改变导致细胞内Ca(2+)信号级联反应某些关键方面出现异常，精神分裂症就可能由多种蛋白质和其他分子的改变引起。
