NeuroMolecular Medicine

, Volume 13, Issue 4, pp 223–250 | Cite as

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

  • Zhiyou Cai
  • Bin Zhao
  • Anna Ratka
Review Paper


Oxidative stress has been proposed to be an important factor in the pathogenesis of Alzheimer’s disease (AD) and contributed to β-amyloid (Aβ) generation. Interaction between oxidative stress and neuro-inflammation leads to Aβ generation. AD is associated with an increase in blood–brain barrier (BBB) permeability due to tight junction involvement. Oxidative stress decreases the expression of low-density lipoprotein receptor-related protein 1 and up-regulates receptor for advanced glycation end products in BBB and increases the BBB permeability, which could potentially lead to increased deposition of Aβ within AD brain. Apoptosis takes place in the pathogenesis of AD, and oxidative stress contributes to apoptosis through both extrinsic pathway and intrinsic pathway. Oxidative stress-induced apoptosis may be a potential factor to Aβ generation. Aβ generation requires two sequential cleavages of APP, with the two proteolytic enzymes: β-secretase and γ-secretase. Oxidative damage up-regulates Aβ via inducing activity of β- and γ-secretases. In this review, we will focus on the mechanism and pathway that oxidative stress contributes to Aβ generation.


Alzheimer’s disease β-Amyloid protein Oxidative stress 





Alzheimer’s disease


Aging, demographics, and memory study


Advanced glycation end products


Amnestic mild cognitive impairment


Ativator protein 1


Amyloid precursor protein




Beta-site APP-cleaving enzyme


Blood–brain barrier


Cerebral nervous system


Extracellular matrix


Glutathione peroxidase Se-dependent




Glycogen synthase kinase 3beta


Human astroglial








Interleukin-1 receptor-associated kinase


Iron-responsive element


Low-density lipoprotein receptor-related protein 1


Mitogen-activated protein kinase


Mild cognitive impairment


Monocyte chemotactic protein 1




Matrix metalloproteinases




Nuclear factor-kappa B


Neurofibrillary tangles


Nervous growth factor


Nitric oxide




Receptor for advanced glycation end products


Reactive nitrogen species


Reactive oxygen species


Senile plaque


Transforming growth factor


Tissue inhibitor of metalloproteinase


Tumor necrosis factor-alpha


Tumor necrosis factor receptor


TNF-receptor-associated death domain



We thank Professor Lin Lu (Department of Pathology, University of Kansas Medical Center, KUMC) for his encouragement and opinion and Dr. Hongren Wang and Dr. Chunhua Li (KUMC) for designing help. This work was supported by the National Nature Science Foundation of China (81070878/H0902) to Dr. Bin Zhao and Start-up Funds from Texas A&M HSC to Dr. Anna Ratka.


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© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Department of Neurology, The Affiliated HospitalGuangdong Medical CollegeXiashan District, ZhanjiangPeople’s Republic of China
  2. 2.Department of Pharmaceutical Sciences, Irma Lerma Rangel College of PharmacyTexas A&M Health Science CenterKingsvilleUSA

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