Oxidative Stress as a Therapeutic Target in Amyotrophic Lateral Sclerosis: Opportunities and Limitations

被引:24
|
作者
Park, Hee Ra [1 ]
Yang, Eun Jin [1 ]
机构
[1] Korea Inst Oriental Med KIOM, KM Med Sci Res Div, Daejeon 34054, South Korea
基金
新加坡国家研究基金会;
关键词
amyotrophic lateral sclerosis; Lou Gehrig's disease; motor neuron disease; oxidative stress; inflammation; reactive oxygen species; superoxide dismutase 1; antioxidants; therapeutics; phytochemicals; MOTOR-NEURON DEGENERATION; ACTIVATED PROTEIN-KINASE; VITAMIN-E INTAKE; MOUSE MODEL; NADPH OXIDASE; SPINAL-CORD; LIPID-PEROXIDATION; UP-REGULATION; DOUBLE-BLIND; DISEASE;
D O I
10.3390/diagnostics11091546
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease (MND) and Lou Gehrig's disease, is characterized by a loss of the lower motor neurons in the spinal cord and the upper motor neurons in the cerebral cortex. Due to the complex and multifactorial nature of the various risk factors and mechanisms that are related to motor neuronal degeneration, the pathological mechanisms of ALS are not fully understood. Oxidative stress is one of the known causes of ALS pathogenesis. This has been observed in patients as well as in cellular and animal models, and is known to induce mitochondrial dysfunction and the loss of motor neurons. Numerous therapeutic agents have been developed to inhibit oxidative stress and neuroinflammation. In this review, we describe the role of oxidative stress in ALS pathogenesis, and discuss several anti-inflammatory and anti-oxidative agents as potential therapeutics for ALS. Although oxidative stress and antioxidant fields are meaningful approaches to delay disease progression and prolong the survival in ALS, it is necessary to investigate various animal models or humans with different subtypes of sporadic and familial ALS.
引用
收藏
页数:16
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