The Relationship Between Brain Aging and Preclinical Alzheimer's Disease

被引:3
|
作者
Chui De-Hua [1 ]
Tian Xiao-Sheng
Wang He-Cheng
Wang Wei
Xiao Wei-Zhong
Fan Dong-Sheng
机构
[1] Peking Univ, Hosp 3, Neurosci Res Inst, Beijing 100191, Peoples R China
基金
中国国家自然科学基金;
关键词
brain aging; preclinical Alzheimer's disease (PCAD); beta-amyloid (A beta); p-Tau; AMYLOID-BETA; COGNITIVE IMPAIRMENT; NEURODEGENERATION; NEURONS; AGGREGATION; BIOMARKERS; DIAGNOSIS; PROGRESS; PATHWAY; ADAM10;
D O I
10.3724/SP.J.1206.2012.00351
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This article reviews the relationship between brain aging and Alzheimer's disease (AD). Specific issues addressed include the question of whether AD and brain aging should be conceptually lumped or split, the extent to which AD and brain aging potentially share common molecular mechanisms, whether beta amyloid should be primarily considered a marker of AD or simply brain aging, and the definition of AD itself. A small percentage of individuals with normal antemortem psychometric scores meet the neuropathological criteria for AD termed "preclinical" AD (PCAD). PCAD and control subjects were compared for oxidative stress markers, amyloid beta-peptide, and identification of protein expression differences, and observed a significant increase in highly insoluble monomeric A beta 42, but no significant differences in oligomeric A beta nor in oxidative stress measurements between controls and PCAD subjects. Expression proteomics identified proteins whose trends in PCAD are indicative of cellular protection, possibly correlating with previous studies showing no cell loss in PCAD.
引用
收藏
页码:741 / 746
页数:6
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