Brain Research Institute, University of Zurich, Zurich, Switzerland.
Neurobiol Dis. 2013 Jun;54:150-7. doi: 10.1016/j.nbd.2013.01.011. Epub 2013 Jan 28.
The membrane protein Nogo-A and its receptor NgR have been extensively characterized for their role in restricting axonal growth, regeneration, and plasticity in the central nervous system. Recent evidence suggests that Nogo and NgR might constitute candidate genes for schizophrenia susceptibility. In this article, we critically review the possibility that dysfunctions related to Nogo-A and NgR might contribute to increased risk for schizophrenia. To this end, we consider the most important insights that have emerged from human genetic and pathological studies and from experimental animal work. Furthermore, we discuss potential mechanisms of Nogo/NgR involvement in neural circuit development and stability, and how mutations or changes in expression levels of these proteins could be developmental risk factors contributing to schizophrenia.
神经突生长抑制因子-A(Nogo-A)及其受体 NgR 在中枢神经系统中对轴突生长、再生和可塑性的限制作用已得到广泛研究。最近的证据表明,Nogo 和 NgR 可能构成精神分裂症易感性的候选基因。在本文中,我们批判性地审查了与 Nogo-A 和 NgR 相关的功能障碍可能导致精神分裂症风险增加的可能性。为此,我们考虑了从人类遗传和病理学研究以及实验动物工作中得出的最重要的见解。此外,我们讨论了 Nogo/NgR 参与神经回路发育和稳定性的潜在机制,以及这些蛋白质的突变或表达水平变化如何成为导致精神分裂症的发育风险因素。