title: Oxidative stress: A major pathogenesis and potential therapeutic target of antioxidative agents in Parkinson's disease and Alzheimer's disease.
abstract: Oxidative stress reflects an imbalance between the overproduction and incorporation of free radicals and the dynamic ability of a biosystem to detoxify reactive intermediates. Free radicals produced by oxidative stress are one of the common features in several experimental models of diseases. Free radicals affect both the structure and function of neural cells, and contribute to a wide range of neurodegenerative diseases, including Parkinson's disease and Alzheimer's disease. Although the precise mechanisms that result in the degeneration of neurons and the relevant pathological changes remain unclear, the crucial role of oxidative stress in the pathogenesis of neurodegenerative diseases is associated with several proteins (such as α-synuclein, DJ-1, Amyloid β and tau protein) and some signaling pathways (such as extracellular regulated protein kinases, phosphoinositide 3-kinase/Protein Kinase B pathway and extracellular signal-regulated kinases 1/2) that are tightly associated with the neural damage. In this review, we present evidence, gathered over the last decade, concerning a variety of pathogenic proteins, their important signaling pathways and pathogenic mechanisms associated with oxidative stress in Parkinson's disease and Alzheimer's disease. Proper control and regulation of these proteins' functions and the related signaling pathways may be a promising therapeutic approach to the patients. We also emphasizes antioxidative options, including some new neuroprotective agents that eliminate excess reactive oxygen species efficiently and have a certain therapeutic effect; however, controversy surrounds some of them in terms of the dose and length of therapy. These agents require further investigation by clinical application in patients suffering Parkinson's disease and Alzheimer's disease.
authors: Department of Neurology, Institute of Neurology and the Collaborative Innovation Center for Brain Science, Rui Jin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
authors: Tianfang
authors: T
authors: Jiang
authors: Department of Neurology, Institute of Neurology and the Collaborative Innovation Center for Brain Science, Rui Jin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
authors: Qian
authors: Q
authors: Sun
authors: Department of Neurology, Institute of Neurology and the Collaborative Innovation Center for Brain Science, Rui Jin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Laboratory of Neurodegenerative Diseases, Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Science & Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. Electronic address: chen_sd@medmail.com.cn.
authors: Shengdi
authors: S
authors: Chen
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism*; D000975:Antioxidants / Q000627:therapeutic use*; D006801:Humans; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010300:Parkinson Disease / Q000188:drug therapy / Q000378:metabolism*
chemical_list: D000975:Antioxidants
keywords: Antioxidative agent; Mitochondria; NADPH oxidase; Neurodegenerative disease; Oxidative stress; Signaling pathway