Oxidative stress in Alzheimer’s disease

• Published in: BBA - Molecular Basis of Disease 2000-07, Vol.1502 (1), p.139-144
• Main Authors: Smith, Mark A., Rottkamp, Catherine A., Nunomura, Akihiko, Raina, Arun K., Perry, George
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - etiology; Alzheimer Disease - prevention & control; Amyloid beta-Peptides - metabolism; Amyloid-β; Antioxidant; Antioxidants - therapeutic use; Free radical; Free Radicals - metabolism; Humans; Mitochondria; Neurofibrillary Tangles - metabolism; Neurons - metabolism; Oxidation-Reduction - drug effects; Oxidative Stress - drug effects; Peptide Fragments - metabolism; Plaque, Amyloid - metabolism; Redox imbalance; Transition metal
• ISSN: 0925-4439; 0006-3002; 1879-260X
• DOI: 10.1016/S0925-4439(00)00040-5

Oxidative balance is emerging as an important issue in understanding the pathogenesis of Alzheimer’s disease. Examination of Alzheimer’s disease brain has demonstrated a great deal of oxidative damage, associated with both hallmark pathologies (senile plaques and neurofibrillary tangles) as well as in normal appearing pyramidal neurons. While this suggests that oxidative stress is a proximal event in Alzheimer’s disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-β-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer’s disease pathogenesis and novel therapeutic approaches.