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本文引用的文献

1
Alzheimer's-related endosome dysfunction in Down syndrome is Abeta-independent but requires APP and is reversed by BACE-1 inhibition.唐氏综合征中与阿尔茨海默病相关的内体功能障碍与 Aβ 无关，但需要 APP，并可被 BACE-1 抑制所逆转。
Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1630-5. doi: 10.1073/pnas.0908953107. Epub 2009 Dec 28.
2
Neuropathology and the neuroinflammation idea.神经病理学与神经炎症学说。
J Alzheimers Dis. 2009;18(3):473-81. doi: 10.3233/JAD-2009-1158.
3
The coming of age of axonal neurotrophin signaling endosomes.轴突神经营养因子信号内体的成熟
J Proteomics. 2009 Feb 15;72(1):46-55. doi: 10.1016/j.jprot.2008.10.007. Epub 2008 Nov 6.
4
Relationships between expression of apolipoprotein E and beta-amyloid precursor protein are altered in proximity to Alzheimer beta-amyloid plaques: potential explanations from cell culture studies.在阿尔茨海默病β-淀粉样蛋白斑块附近，载脂蛋白E与β-淀粉样前体蛋白的表达关系发生改变：来自细胞培养研究的潜在解释。
J Neuropathol Exp Neurol. 2008 Aug;67(8):773-83. doi: 10.1097/NEN.0b013e318180ec47.
5
APP duplication is sufficient to cause early onset Alzheimer's dementia with cerebral amyloid angiopathy.APP基因重复足以导致早发性阿尔茨海默病性痴呆伴脑淀粉样血管病。
Brain. 2006 Nov;129(Pt 11):2977-83. doi: 10.1093/brain/awl203. Epub 2006 Aug 18.
6
Lysosomal system pathways: genes to neurodegeneration in Alzheimer's disease.溶酶体系统途径：阿尔茨海默病中导致神经退行性变的基因
J Alzheimers Dis. 2006;9(3 Suppl):277-89. doi: 10.3233/jad-2006-9s331.
7
Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration.唐氏综合征小鼠模型中App表达增加会破坏神经生长因子（NGF）的运输并导致胆碱能神经元变性。
Neuron. 2006 Jul 6;51(1):29-42. doi: 10.1016/j.neuron.2006.05.022.
8
Promoter mutations that increase amyloid precursor-protein expression are associated with Alzheimer disease.增加淀粉样前体蛋白表达的启动子突变与阿尔茨海默病相关。
Am J Hum Genet. 2006 Jun;78(6):936-46. doi: 10.1086/504044. Epub 2006 Apr 10.
9
APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy.APP基因座重复导致常染色体显性遗传的早发性阿尔茨海默病伴脑淀粉样血管病。
Nat Genet. 2006 Jan;38(1):24-6. doi: 10.1038/ng1718. Epub 2005 Dec 20.
10
Glia and their cytokines in progression of neurodegeneration.神经胶质细胞及其细胞因子在神经退行性变进展中的作用
Neurobiol Aging. 2005 Mar;26(3):349-54. doi: 10.1016/j.neurobiolaging.2004.05.010.

Excess betaCTF, not Abeta: the culprit in Alzheimer-related endocytic dysfunction.

作者信息

Griffin W Sue T

机构信息

Donald W. Reynolds Department of Geriatrics and Institute on Aging, University of Arkansas for Medical Sciences, and the GRECC at the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA.

出版信息

Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1263-4. doi: 10.1073/pnas.0913922107.

DOI:10.1073/pnas.0913922107
PMID:20133888
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2824414/
Abstract
摘要