Oxidative stress in Alzheimer's disease.
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-beta-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.
Smith
M A
MA
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA. mas21@po.cwru.edu
Rottkamp
C A
CA
Nunomura
A
A
Raina
A K
AK
Perry
G
G
D000544:Alzheimer Disease / Q000209:etiology* / Q000517:prevention & control; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000975:Antioxidants / Q000627:therapeutic use; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D016874:Neurofibrillary Tangles / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D010446:Peptide Fragments / Q000378:metabolism; D058225:Plaque, Amyloid / Q000378:metabolism
D016229:Amyloid beta-Peptides; D000975:Antioxidants; D005609:Free Radicals; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)