Abstract
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.
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Abbreviations
- Aβ :
-
β-Amyloid
- AD:
-
Alzheimer’s disease
- ADAMS:
-
Aging, demographics, and memory study
- AGEs:
-
Advanced glycation end products
- aMCI:
-
Amnestic mild cognitive impairment
- AP-1:
-
Ativator protein 1
- APP:
-
Amyloid precursor protein
- AS:
-
Astrocyte
- BACE:
-
Beta-site APP-cleaving enzyme
- BBB:
-
Blood–brain barrier
- CNS:
-
Cerebral nervous system
- ECM:
-
Extracellular matrix
- GPx-Se:
-
Glutathione peroxidase Se-dependent
- GSH:
-
Glulathione
- GSK-3β :
-
Glycogen synthase kinase 3beta
- HAG:
-
Human astroglial
- HPA:
-
Hypothalamus–pituitary–adrenal
- IFN:
-
Interferon
- IL:
-
Interleukin
- IRAK:
-
Interleukin-1 receptor-associated kinase
- IRE:
-
Iron-responsive element
- LRP-1:
-
Low-density lipoprotein receptor-related protein 1
- MAPK:
-
Mitogen-activated protein kinase
- MCI:
-
Mild cognitive impairment
- MCP-1:
-
Monocyte chemotactic protein 1
- MG:
-
Microglia
- MMPs:
-
Matrix metalloproteinases
- NMDA:
-
N-Methyl-d-aspartate
- NF-κB:
-
Nuclear factor-kappa B
- NFT:
-
Neurofibrillary tangles
- NGF:
-
Nervous growth factor
- NO:
-
Nitric oxide
- NT-3:
-
Neurotrofin-3
- RAGE:
-
Receptor for advanced glycation end products
- RNS:
-
Reactive nitrogen species
- ROS:
-
Reactive oxygen species
- SP:
-
Senile plaque
- TGF:
-
Transforming growth factor
- TIMP:
-
Tissue inhibitor of metalloproteinase
- TNF-α :
-
Tumor necrosis factor-alpha
- TNFR:
-
Tumor necrosis factor receptor
- TRADD:
-
TNF-receptor-associated death domain
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Acknowledgments
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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Cai, Z., Zhao, B. & Ratka, A. Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease. Neuromol Med 13, 223–250 (2011). https://doi.org/10.1007/s12017-011-8155-9
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DOI: https://doi.org/10.1007/s12017-011-8155-9