Oxidative stress as a biomarker for Alzheimer's disease

被引:45
作者
Collin, Fabrice [1 ,2 ]
Cheignon, Clemence [1 ,2 ,3 ]
Hureau, Christelle [1 ,2 ]
机构
[1] CNRS, UPR 8241, LCC, 205 Route Narbonne, F-31062 Toulouse 09, France
[2] Univ Toulouse, UPS, INPT, F-31077 Toulouse, France
[3] Univ Montpellier, IBMM, F-34095 Montpellier 5, France
关键词
Alzheimer's disease; amyloid beta peptide; lipid peroxidation; oxidative stress; peripheral biofluids; tau protein; MILD COGNITIVE IMPAIRMENT; AMYLOID-BETA-PEPTIDE; BRAIN; DIAGNOSIS;
D O I
10.2217/bmm-2017-0456
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
It is estimated that Alzheimer's disease (AD) is striking 1 in 20 over age 65, which yielded to 23-35 million people worldwide in 2015. The number of AD victims is expected to almost double every 20 years, thus placing the national healthcare systems under dramatically increasing pressure. This clearly underlines the need to find early biomarkers and efficient medical treatments for AD, both implying a better understanding of the mechanism from the origin of the disease to the death of the neurons. Oxidative damages on neuronal lipids and proteins, in particular, are an important feature of AD and a link with oxidative stress [1]. The latter can have different origins, but the overproduction of reactive oxygen species (ROS) is considered as a major contribution. Loosely bound metal ions (copper and iron), present in the brain and at high concentration in senile plaques of AD patients, may bind to the amyloid beta peptide (A beta) thus catalyzing very efficiently the production of ROS (in particular, the oligomeric forms of A beta, known as being the most toxic). This represents one of the source for ROS production in brain, a second one being mitochondria dysfunction.
引用
收藏
页码:201 / 203
页数:3
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