Department of Neurology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
J Neural Transm (Vienna). 2024 Jun;131(6):597-607. doi: 10.1007/s00702-024-02788-w. Epub 2024 Jun 12.
For a special issue, we review studies on the pathogenesis of nigral cell death and the treatment of sporadic Parkinson's disease (sPD) over the past few decades, with a focus on the studies performed by Prof. Mizuno and our group. Prof. Mizuno proposed the initial concept that mitochondrial function may be impaired in sPD. When working at Jichi Medical School, he found a decrease in complex I of the mitochondrial electron transfer complex in the substantia nigra of patients with Parkinson's disease (PD) and MPTP models. After moving to Juntendo University as a professor and chairman, he continued to study the mechanisms of cell death in the substantia nigra of patients with sPD. Under his supervision, I studied the relationships between PD and apoptosis, PD and iron involvement, mitochondrial dysfunction and apoptosis, and PD and neuroinflammation. Moving to Kitasato University, we focused on PD and the cytotoxicity of alpha synuclein (αSyn) as well as brain neuropathology. Eventually, I moved to Osaka University, where I continued working on PD and αSyn projects to promote therapeutic research. In this paper, we present the details of these studies in the following order: past, present, and future.
为了一期特刊，我们回顾了过去几十年中关于黑质细胞死亡的发病机制和散发性帕金森病（sPD）治疗的研究，重点介绍了 Mizuno 教授和我们小组的研究。Mizuno 教授提出了线粒体功能可能在 sPD 中受损的最初概念。在筑波大学医学科学研究所工作时，他发现帕金森病（PD）患者和 MPTP 模型的黑质中线粒体电子传递复合物 I 复合物减少。调到顺天堂大学担任教授和主席后，他继续研究 sPD 患者黑质细胞死亡的机制。在他的指导下，我研究了 PD 与细胞凋亡、PD 与铁参与、线粒体功能障碍与细胞凋亡以及 PD 与神经炎症之间的关系。搬到了北里大学，我们专注于 PD 和毒性α-突触核蛋白（αSyn）以及脑病理学。最终，我搬到了大阪大学，继续从事 PD 和αSyn 项目的研究，以促进治疗研究。在本文中，我们按照过去、现在和未来的顺序介绍了这些研究的详细信息。
