当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い
。オープンアクセスジャーナルはより多くの読者と引用を獲得
700 ジャーナル と 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得
Zixuan Chen, Jianqing Lu, Jinyan Duan, Xiaotong Zheng, Yanyan Zhang, Chao Han and Yulin Deng*
Parkinson disease (PD) is the second most common neurodegenerative disorder after Alzheimer disease with no definitive neuroprotective therapies. Previous studies have demonstrated that Catechol tetra hydroisoquinolines (CTIQs) are toxic to dopaminergic neurons. These toxins can induce mitochondrial dysfunction, which consequently contributes to the pathogenesis of PD. Unlike external neurotoxins, such as agrochemicals and MPTP, CTIQs can be synthesized in the brains of human based on the dopamine and the particular aldehyde. Besides, aggregated α-synuclein (α-syn), one of the hallmarks of PD, has been proved to be a key contributor in the development of PD and can be affected by many neurotoxins. Some studies have presented that CTIQs enhanced the aggregation of α-syn and increased the neurotoxin of α-syn, which might be the pathological mechanism of PD. Therefore, this chapter will reveal the role of CTIQs and α-syn and try to clarify the relationship between them.