A standard model of Alzheimer's disease?

被引:13
|
作者
Walker, Lary C. [1 ,2 ]
Lynn, David G. [3 ,4 ]
Chernoff, Yury O. [5 ,6 ,7 ]
机构
[1] Emory Univ, Dept Neurol, 505M Whitehead Bldg,615 Michael St, Atlanta, GA 30322 USA
[2] Emory Univ, Yerkes Natl Primate Res Ctr, 505M Whitehead Bldg,615 Michael St, Atlanta, GA 30322 USA
[3] Emory Univ, Dept Biol, Atlanta, GA 30322 USA
[4] Emory Univ, Dept Chem, 1515 Pierce Dr, Atlanta, GA 30322 USA
[5] Georgia Inst Technol, Sch Biol Sci, Atlanta, GA 30332 USA
[6] St Petersburg State Univ, Lab Amyloid Biol, St Petersburg, Russia
[7] St Petersburg State Univ, Inst Translat Biomed, St Petersburg, Russia
基金
美国国家卫生研究院; 美国国家科学基金会; 俄罗斯科学基金会;
关键词
Abeta; Alzheimer; amyloid; aging; dementia; neurodegeneration; prion; proteopathy; seeding; tau; BETA; TAU; PROPAGATION; PROGRESSION; CHICKEN; LONG;
D O I
10.1080/19336896.2018.1525256
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
The recent Research Framework proposed by the US National Institute on Aging and the Alzheimer's Association (NIA-AA) recommends that Alzheimer's disease be defined by its specific biology rather than by non-specific neurodegenerative and syndromal features. By affirming markers of abnormal A beta and tau proteins as the essential pathobiological signature of Alzheimer's disease, the Framework tacitly reinforces the amyloid (A beta) cascade as the leading theory of Alzheimer pathogenesis. In light of recent evidence that the cascade is driven by the misfolding and templated aggregation of A beta and tau, we believe that an empirically grounded Standard Model of Alzheimer's pathogenesis is within reach. A Standard Model can clarify and consolidate existing information, contextualize risk factors and the complex disease phenotype, identify testable hypotheses for future research, and pave the most direct path to effective prevention and treatment.
引用
收藏
页码:261 / 265
页数:5
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