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The Alzheimer family of diseases: many etiologies, one pathogenesis?阿尔茨海默病家族性疾病:多种病因,一种发病机制?
Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2095-7. doi: 10.1073/pnas.94.6.2095.
2
[Alzheimer's disease].[阿尔茨海默病]
Tanpakushitsu Kakusan Koso. 1997 Oct;42(14 Suppl):2393-8.
3
A causal role for amyloid in Alzheimer's disease: the end of the beginning.淀粉样蛋白在阿尔茨海默病中的因果作用:开端的结束。
Neurology. 1993 May;43(5):851-6. doi: 10.1212/wnl.43.5.851.
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Alzheimer's disease or Alzheimer's diseases? Clues from molecular epidemiology.阿尔茨海默病还是多种阿尔茨海默病?来自分子流行病学的线索。
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Amyloidogenic processing of beta-amyloid precursor protein in intracellular compartments.细胞内区室中β-淀粉样前体蛋白的淀粉样生成加工过程。
Neurology. 2006 Jan 24;66(2 Suppl 1):S69-73. doi: 10.1212/01.wnl.0000192107.17175.39.
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7
Molecular genetics of Alzheimer's disease.
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[gamma secretase].
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in Neurodegenerative Disorders: Mutation Spectrum, Pathophysiology, and Therapeutic Targeting.《神经退行性疾病:突变谱、病理生理学及治疗靶点》
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Sleep fragmentation affects glymphatic system through the different expression of AQP4 in wild type and 5xFAD mouse models.睡眠片段化通过在野生型和 5xFAD 小鼠模型中不同表达 AQP4 影响糖胺聚糖系统。
Acta Neuropathol Commun. 2023 Jan 18;11(1):16. doi: 10.1186/s40478-022-01498-2.
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Chronic sleep fragmentation shares similar pathogenesis with neurodegenerative diseases: Endosome-autophagosome-lysosome pathway dysfunction and microglia-mediated neuroinflammation.慢性睡眠碎片化与神经退行性疾病具有相似的发病机制:内体-自噬体-溶酶体途径功能障碍和小胶质细胞介导的神经炎症。
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The Possibility of an Infectious Etiology of Alzheimer Disease.阿尔茨海默病感染病因学的可能性。
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Oil Palm Phenolics Inhibit the Aggregation of -Amyloid Peptide into Oligomeric Complexes.油棕酚类物质抑制β-淀粉样肽聚集成寡聚复合物。
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Early Contextual Fear Memory Deficits in a Double-Transgenic Amyloid- Precursor Protein/Presenilin 2 Mouse Model of Alzheimer's Disease.阿尔茨海默病双转基因淀粉样前体蛋白/早老素2小鼠模型中的早期情境恐惧记忆缺陷
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Maysin and Its Flavonoid Derivative from Centipedegrass Attenuates Amyloid Plaques by Inducting Humoral Immune Response with Th2 Skewed Cytokine Response in the Tg (APPswe, PS1dE9) Alzheimer's Mouse Model.来自假俭草的五月苷及其黄酮类衍生物通过在Tg(APPswe,PS1dE9)阿尔茨海默病小鼠模型中诱导具有Th2偏向性细胞因子反应的体液免疫反应来减轻淀粉样斑块。
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The road to restoring neural circuits for the treatment of Alzheimer's disease.恢复神经回路以治疗阿尔茨海默病的道路。
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本文引用的文献

1
The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid beta protein ending at the 42nd (or 43rd) residue.与家族性阿尔茨海默病(伏尔加德意志人家族)相关的早老素2突变(N141I)增加了以第42(或43)个残基结尾的β淀粉样蛋白的分泌。
Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):2025-30. doi: 10.1073/pnas.94.5.2025.
2
Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice.阿尔茨海默病的突变早老素在转染细胞和转基因小鼠中均会增加42个氨基酸残基的β淀粉样蛋白的产生。
Nat Med. 1997 Jan;3(1):67-72. doi: 10.1038/nm0197-67.
3
Assessment of normal and mutant human presenilin function in Caenorhabditis elegans.秀丽隐杆线虫中正常和突变型人类早老素功能的评估。
Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14940-4. doi: 10.1073/pnas.93.25.14940.
4
Membrane topology of the C. elegans SEL-12 presenilin.秀丽隐杆线虫SEL-12早老素的膜拓扑结构
Neuron. 1996 Nov;17(5):1015-21. doi: 10.1016/s0896-6273(00)80231-7.
5
Familial Alzheimer's disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo.家族性阿尔茨海默病相关的早老素1变体在体外和体内均可提高β淀粉样蛋白1-42/1-40的比例。
Neuron. 1996 Nov;17(5):1005-13. doi: 10.1016/s0896-6273(00)80230-5.
6
Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1.在表达突变型早老素1的小鼠大脑中β淀粉样蛋白42(43)增加。
Nature. 1996 Oct 24;383(6602):710-3. doi: 10.1038/383710a0.
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The presenilin genes: a new gene family involved in Alzheimer disease pathology.早老素基因:一个参与阿尔茨海默病病理学的新基因家族。
Hum Mol Genet. 1996;5 Spec No:1449-55. doi: 10.1093/hmg/5.supplement_1.1449.
8
Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice.转基因小鼠中的相关记忆缺陷、β-淀粉样蛋白升高和淀粉样斑块。
Science. 1996 Oct 4;274(5284):99-102. doi: 10.1126/science.274.5284.99.
9
Amyloid beta protein (Abeta) deposition in chromosome 14-linked Alzheimer's disease: predominance of Abeta42(43).14号染色体连锁的阿尔茨海默病中β淀粉样蛋白(Aβ)沉积:Aβ42(43)占主导地位
Ann Neurol. 1996 Aug;40(2):149-56. doi: 10.1002/ana.410400205.
10
A mutation in Alzheimer's disease destroying a splice acceptor site in the presenilin-1 gene.阿尔茨海默病中的一种突变破坏了早老素-1基因中的一个剪接受体位点。
Neuroreport. 1995 Dec 29;7(1):297-301.

The Alzheimer family of diseases: many etiologies, one pathogenesis?

作者信息

Hardy J

机构信息

Mayo Clinic Jacksonville, FL 32084, USA.

出版信息

Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2095-7. doi: 10.1073/pnas.94.6.2095.

DOI:10.1073/pnas.94.6.2095
PMID:9122152
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC33655/
Abstract
摘要