Oxidative Stress and the Pathogenesis of Alzheimer's Disease
By Yan Zhao, Baolu Zhao. Oxidative Medicine and Cellular Longevity, 2013
783 citations recorded by the source corpus.
Alzheimer's disease (AD) is the most common neurodegenerative disease that causes dementia in the elderly. Patients with AD suffer a gradual deterioration of memory and other cognitive functions, which eventually leads to a complete incapacity and death. A complicated array of molecular events has been implicated in the pathogenesis of AD. The major pathological characteristics of AD brains are the presence of senile plaques, neurofibrillary tangles, and neuronal loss. Growing evidence has demonstrated that oxidative stress is an important factor contributing to the initiation and progression of AD. However, the mechanisms that lead to the disruption of redox balance and the sources of free radicals remain elusive. The excessive reactive oxygen species may be generated from mechanisms such as mitochondria dysfunction and/or aberrant accumulation of transition metals, while the abnormal accumulation of Abeta and tau proteins appears to promote the redox imbalance. The resulted oxidative stress has been implicated in Abeta- or tau-induced neurotoxicity. In addition, evidence has suggested that oxidative stress may augment the production and aggregation of Abeta and facilitate the phosphorylation and polymerization of tau, thus forming a vicious cycle that promotes the initiation and progression of AD.
Subfields: Nutrition and Dietetics, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/eb6f5354966b3e5fdf7bf58ed21ee9dea34a6403
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Citations in the corpus
- Oxidative stress and the amyloid beta peptide in Alzheimer’s disease (2017, background): “In addition to ROS production by Aβ peptides in the presence of metal ions (see the section “Aβ peptide and ROS production” below), mitochondria dysfunction has also been involved in AD pathogenesis, via mitochondrial ROS generation [54,55].”
- Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders (2017, background): “the succession of AD.[27] Vascular dysfunction, including reduced cerebral blood flow (CBF), disturbance in blood–brain barrier (BBB) and cerebral amyloid angiopathy are also reported in AD.”
- Oxidative stress, mitochondrial dysfunction and neurodegenerative diseases; a mechanistic insight. (2015, background): “Different evidence has also suggested that oxidative stress may enhance the production and aggregation of Abeta and facilitate the polymerization and phosphorylation of tau and as such forms the vicious cycle that promotes the commencement and succession of AD [54].”
- The Role of Oxidative Stress in Neurodegenerative Diseases (2015, background): “In addition, AD transgenic mouse models expressing mutant amyloid precursor protein (APP) and presenilin-1 (PS-1) have shown increased levels of H2O2 and peroxidation of proteins and lipids, implying that Aβ may enhance oxidative stress in AD [72, 74].”