Abstract
Oxidative stress is an important factor, and one that acts in the earliest stages, of Alzheimer’s disease (AD) pathogenesis. The reduction of oxidative stress has been tested as a therapy for AD. While the trial of vitamin E supplementation in moderately severe AD is the most promising so far, it also reveals the limitations of general antioxidant therapies that simply lower oxidative stress and, therefore, the complexity of the redox system. The multiple contributing factors that foster the clinical manifestations of AD should be considered when designing antioxidative stress therapy. In this article, we discuss the multiple pathogenic mechanisms of oxidative stress in AD and the potential targeting approaches.
Financial & competing interests disclosure
Mark A Smith is, or has in the past been, a paid consultant for, owns equity or stock options in and/or receives grant funding from Anavex, Canopus BioPharma, Medivation, Neurotez, Neuropharm, Panacea Pharmaceuticals and Voyager Pharmaceuticals. George Perry is, or has in the past been, a paid consultant for and/or owns equity or stock options in Neurotez Pharmaceuticals, Panacea Pharmaceuticals, Takeda Pharmaceuticals and Voyager Pharmaceuticals. Xiongwei Zhu is a paid Advisory Board member for Medivation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.