Pathways to Alzheimer's disease

被引:138
|
作者
Hardy, J. [1 ]
Bogdanovic, N. [2 ]
Winblad, B. [3 ]
Portelius, E. [4 ]
Andreasen, N. [3 ]
Cedazo-Minguez, A. [3 ]
Zetterberg, H. [1 ,4 ]
机构
[1] UCL Inst Neurol, Reta Lila Weston Res Labs, Dept Mol Neurosci, London WC1N 3BG, England
[2] Karolinska Inst, Sect Clin Geriatr, Stockholm, Sweden
[3] Karolinska Inst, KI Alzheimer Dis Res Ctr, NVS, Stockholm, Sweden
[4] Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Gothenburg, Sweden
关键词
Alzheimer's disease; amyloid; cell biology; genetics; tau; AMYLOID PRECURSOR PROTEIN; APOLIPOPROTEIN-E; COMPLEMENT ACTIVATION; COMMON VARIANTS; BETA-PEPTIDE; A-BETA; THERAPEUTICS; MECHANISMS; DEPOSITION; ANTIBODY;
D O I
10.1111/joim.12192
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Recent trials of anti-amyloid agents have not produced convincing improvements in clinical outcome in Alzheimer's disease; however, the reason for these poor or inconclusive results remains unclear. Recent genetic data continue to support the amyloid hypothesis of Alzheimer's disease with protective variants being found in the amyloid gene and both common low-risk and rare high-risk variants for disease being discovered in genes that are part of the amyloid response pathways. These data support the view that genetic variability in how the brain responds to amyloid deposition is a potential therapeutic target for the disease, and are consistent with the notion that anti-amyloid therapies should be initiated early in the disease process.
引用
收藏
页码:296 / 303
页数:8
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