Is oxidative damage the fundamental pathogenic mechanism of Alzheimer’s and other neurodegenerative diseases?

• Published in: Free Radical Biology and Medicine Vol. 33; no. 11; pp. 1475 - 1479
• Main Authors: Perry, George, Nunomura, Akihiko, Hirai, Keisuke, Zhu, Xiongwei, Prez, Mar, Avila, Jess, Castellani, Rudolph J, Atwood, Craig S, Aliev, Gjumrakch, Sayre, Lawrence M, Takeda, Atsushi, Smith, Mark A
• Format: Book Review Journal Article
• Language: English
• Published: United States Elsevier Inc 01-12-2002
• Subjects: Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Alzheimer’s disease; Amyloid-β; Animals; Antioxidants; Free Radicals; Homeostasis; Humans; Neurodegenerative Diseases - pathology; Neurofibrillary tangles; Oxidation-Reduction; Oxidative Stress; Reactive Oxygen Species; Redox balance; Senile plaque; Antioxidants; Oxidative stress; Neurofibrillary tangles; Free radicals; Alzheimer’s disease; τ; Senile plaque; Homeostasis; Redox balance; Amyloid-β
• ISSN: 0891-5849; 1873-4596
• DOI: 10.1016/S0891-5849(02)01113-9

In less than a decade, beginning with the demonstration by Floyd, Stadtman, Markesbery et al.
[1] of increased reactive carbonyls in the brains of patients with Alzheimer’s disease (AD), oxidative damage has been established as a feature of the disease. Here, we review the types of oxidative damage seen in AD, sites involved, possible origin, relationship to lesions, and compensatory changes, and we also consider other neurodegenerative diseases where oxidative stress has been implicated. Although much data remain to be collected, the broad spectrum of changes found in AD are only seen, albeit to a lesser extent, in normal aging with other neurodegenerative diseases showing distinct spectrums of change.