Role of reactive oxygen species in the progression of Alzheimer's disease. Issue 3 (March 2021)

• Record Type: Journal Article
• Authors: Bhatt, Shvetank; Puli, Lakshman; Patil, Chandragauda R.
• Is Part Of: Drug discovery today. Volume 26:Issue 3(2021)
• Page Start: 794
• Page End: 803
• Publication Date: 2021-03
• Subjects: Drugs -- Design -- Periodicals; Drugs -- Research -- Periodicals; 615.1
• DOI: 10.1016/j.drudis.2020.12.004
• Languages: English
• ISSNs: 1359-6446

Abstract

Highlights: Oxidative stress is an etiopathogenic event upstream to Aβ-plaques and neurofibrillary tangles leading to Alzheimer's disease. Unquenched ROS perturb the neuronal signaling, trigger pro-inflammatory pathways, and induce neuronal apoptosis/necrosis. Various innate and dietary anti-oxidants are emerging as anti-Alzheimer agents with marginal benefits. Abstract : The pathogenesis of Alzheimer's disease (AD) involves neurodegeneration following the deposition of β-amyloid (Aβ) plaques and neurofibrillary tangles in vulnerable brain regions. The vulnerability of the brain to reactive oxygen species (ROS) is now emerging as a key detrimental factor driving AD pathogenesis. Oxidative stress (OS) irreversibly damages cellular biomolecules and perturbs neuronal functions. Scientific evidence is emerging that supports the therapeutic effects of antioxidants in preventing the onset and delaying the progression of AD pathology. In this review, we highlight the role of the OS in AD and the importance of antioxidants in its treatment.