Compensatory responses induced by oxidative stress in Alzheimer disease.
Oxidative stress occurs early in the progression of Alzheimer disease, significantly before the development of the pathologic hallmarks, neurofibrillary tangles and senile plaques. In the first stage of development of the disease, amyloid-beta deposition and hyperphosphorylated tau function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. These findings suggest that Alzheimer disease is associated with a novel balance in oxidant homeostasis.
Moreira
Paula I
PI
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44100, USA.
Zhu
Xiongwei
X
Liu
Quan
Q
Honda
Kazuhiro
K
Siedlak
Sandra L
SL
Harris
Peggy L
PL
Smith
Mark A
MA
Perry
George
G
D000222:Adaptation, Physiological; D000544:Alzheimer Disease / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D018450:Disease Progression; D038362:Glycogen Synthase Kinase 3; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D009474:Neurons / Q000502:physiology*; D010085:Oxidative Phosphorylation; D018384:Oxidative Stress / Q000502:physiology*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*
D016229:Amyloid beta-Peptides; D017346:Protein Serine-Threonine Kinases; D038362:Glycogen Synthase Kinase 3; C080888:tau-protein kinase