Year: 2013
Type: review
Abstract: 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.
DOI: 10.1155/2013/316523
Authors: Yan Zhao, Baolu Zhao
Language: English
Subfield: Cellular and Molecular Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $2,680
Awards: G1056934724, G1127964627, G1197894918, G184922271, G1910816300, G2042286075, G2233382362, G2285018905, G2472442579, G2678018968, G2682269640, 帕金森病黑质内铁选择性聚集并特异性损伤多巴胺能神经元的机制及防治研究, G2826232515, G3068590645, G318702426, G4069041175, G4163519237, G4199803825, G4266073293, G487718006, G5159117605, G5275732665, G5506029551, G6279619195, G693906830, G7287874643, G7400929702, G7413655639, G7428426999, G7442627826, G7494009872, G8023676483, G8100857545, G8301798819
OpenAlex ID: W2141262291
