Luke Molinaro, Patricia Hui, Mattea Tan, Ram K Mishra, Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario L8N 3Z5, Canada.
World J Psychiatry. 2015 Sep 22;5(3):260-72. doi: 10.5498/wjp.v5.i3.260.
Synapsin II is a member of the neuronal phosphoprotein family. These phosphoproteins are evolutionarily conserved across many organisms and are important in a variety of synaptic functions, including synaptogenesis and the regulation of neurotransmitter release. A number of genome-wide scans, meta-analyses, and genetic susceptibility studies have implicated the synapsin II gene (3p25) in the etiology of schizophrenia (SZ) and other psychiatric disorders. Further studies have found a reduction of synapsin II mRNA and protein in the prefrontal cortex in post-mortem samples from schizophrenic patients. Disruptions in the expression of this gene may cause synaptic dysfunction, which can result in neurotransmitter imbalances, likely contributing to the pathogenesis of SZ. SZ is a costly, debilitating psychiatric illness affecting approximately 1.1% of the world's population, amounting to 51 million people today. The disorder is characterized by positive (hallucinations, paranoia), negative (social withdrawal, lack of motivation), and cognitive (memory impairments, attention deficits) symptoms. This review provides a comprehensive summary of the structure, function, and involvement of the synapsin family, specifically synapsin II, in the pathophysiology of SZ and possible target for therapeutic intervention/implications.
突触结合蛋白 II 是神经元磷酸化蛋白家族的一员。这些磷酸化蛋白在许多生物中具有进化保守性，在各种突触功能中都很重要，包括突触发生和神经递质释放的调节。许多全基因组扫描、荟萃分析和遗传易感性研究都表明突触结合蛋白 II 基因（3p25）与精神分裂症（SZ）和其他精神障碍的病因有关。进一步的研究发现，精神分裂症患者死后的前额叶皮质中突触结合蛋白 II mRNA 和蛋白减少。该基因表达的中断可能导致突触功能障碍，从而导致神经递质失衡，可能导致 SZ 的发病机制。SZ 是一种代价高昂、使人衰弱的精神疾病，影响着全球约 1.1%的人口，目前全球有 5100 万人患有这种疾病。该疾病的特征是阳性（幻觉、妄想）、阴性（社会退缩、缺乏动力）和认知（记忆障碍、注意力缺陷）症状。本文全面总结了突触结合蛋白家族，特别是突触结合蛋白 II，在 SZ 病理生理学中的结构、功能和作用，以及作为治疗干预的可能靶点/意义。
