Alzheimer Disease and the Role of Free Radicals in the Pathogenesis of the Disease

Author(s): George Perry, Paula I. Moreira, Maria S. Santos, Catarina R. Oliveira, Justin C. Shenk, Akihiko Nunomura, Mark A. Smith, Xiongwei Zhu.

Journal Name: CNS & Neurological Disorders - Drug Targets
(Formerly Current Drug Targets - CNS & Neurological Disorders)

Volume 7 , Issue 1 , 2008

Become EABM
Become Reviewer


Oxidative stress occurs early in the progression of Alzheimer disease, significantly before the development of the pathologic hallmarks, neurofibrillary tangles and senile plaques. All classes of macromolecules (sugar, lipids, proteins, and nucleic acids) are affected by oxidative stress leading, inevitably, to neuronal dysfunction. Extensive data from the literature support the notion that mitochondrial and metal abnormalities are key sources of oxidative stress in Alzheimer disease. Furthermore, it has been suggested that in the initial stages of the development of Alzheimer disease, amyloid-β deposition and hyperphosphorylated tau function as compensatory responses to ensure that neuronal cells do not succumb to oxidative damage. However, during the progression of the disease, the antioxidant activity of both agents is either overwhelmed or, according to others, evolves into pro-oxidant activity resulting in the exacerbation of reactive species production.

Keywords: Alzheimer disease, antioxidant, chelator, iron, mitochondria, oxidative stress, reactive oxygen species

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2008
Page: [3 - 10]
Pages: 8
DOI: 10.2174/187152708783885156

Article Metrics

PDF: 32