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本文引用的文献

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Perivascular drainage of amyloid-beta peptides from the brain and its failure in cerebral amyloid angiopathy and Alzheimer's disease.淀粉样β肽从脑内的血管周围引流及其在脑淀粉样血管病和阿尔茨海默病中的功能障碍
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Cystatin C modulates cerebral beta-amyloidosis.胱抑素C调节脑内β-淀粉样变性。
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Familial Alzheimer's disease mutations alter the stability of the amyloid beta-protein monomer folding nucleus.家族性阿尔茨海默病突变会改变淀粉样β蛋白单体折叠核的稳定性。
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Cerebral vascular accumulation of Dutch-type Abeta42, but not wild-type Abeta42, in hereditary cerebral hemorrhage with amyloidosis, Dutch type.在荷兰型遗传性脑出血伴淀粉样变性中，脑血管中存在荷兰型β淀粉样蛋白42（Abeta42）的蓄积，而野生型Abeta42则不存在。
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BACE1 and mutated presenilin-1 differently modulate Abeta40 and Abeta42 levels and cerebral amyloidosis in APPDutch transgenic mice.β-分泌酶1（BACE1）和突变型早老素-1对荷兰型淀粉样前体蛋白（APP）转基因小鼠的β淀粉样蛋白40（Aβ40）和β淀粉样蛋白42（Aβ42）水平及脑淀粉样变性有不同的调节作用。
Neurodegener Dis. 2007;4(2-3):127-35. doi: 10.1159/000101837.
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Abeta40 protects non-toxic Abeta42 monomer from aggregation.淀粉样前体蛋白40（Abeta40）可保护无毒的淀粉样前体蛋白42（Abeta42）单体不发生聚集。
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Abeta40 inhibits amyloid deposition in vivo.β淀粉样蛋白40在体内抑制淀粉样蛋白沉积。
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Mean age-of-onset of familial alzheimer disease caused by presenilin mutations correlates with both increased Abeta42 and decreased Abeta40.由早老素突变引起的家族性阿尔茨海默病的平均发病年龄与β淀粉样蛋白42增加和β淀粉样蛋白40减少均相关。
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Mechanism of cerebral beta-amyloid angiopathy: murine and cellular models.脑β-淀粉样血管病的机制：小鼠和细胞模型
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E22Q突变型β-淀粉样肽（荷兰型β-淀粉样肽）增加血管中β-淀粉样蛋白沉积，但减少实质组织中β-淀粉样蛋白沉积。

E22Q-mutant Abeta peptide (AbetaDutch) increases vascular but reduces parenchymal Abeta deposition.

作者信息

Herzig Martin C, Eisele Yvonne S, Staufenbiel Matthias, Jucker Mathias

机构信息

Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Otfried-Müller Strasse 27, D-72076 Tübingen, Germany.

出版信息

Am J Pathol. 2009 Mar;174(3):722-6. doi: 10.2353/ajpath.2009.080790. Epub 2009 Feb 13.

DOI:10.2353/ajpath.2009.080790
PMID:19218342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2665734/
Abstract

Patients that have hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D) generate both wild-type beta-amyloid (Abetawt) and E22Q-mutant beta-amyloid (AbetaDutch). Postmortem analysis of HCHWA-D brains reveals severe cerebral amyloid angiopathy with very little parenchymal amyloid deposition. To investigate amyloidosis in the presence of both Abetawt and AbetaDutch variants, transgenic (tg) APP23 mice were crossed with APPDutch mice. Although single-tg APP23 mice deposited Abetawt with aging, double-tg APP23/APPDutch mice co-deposited AbetaDutch (mainly AbetaDutch1-40) and Abetawt at twofold higher total Abeta levels. Vascular Abeta deposits and hemorrhages were twice as high in APP23/APPDutch mice compared with APP23 mice. Surprisingly, parenchymal Abeta deposition was reduced in the double-tg mice compared with the single-tg APP23 mice. Our findings suggest that AbetaDutch1-40 inhibits parenchymal amyloidosis but exacerbates vascular amyloid, hence explaining the compartment-specific distribution of cerebral amyloid in HCHWA-D patients.

摘要

患有荷兰型遗传性脑出血伴淀粉样变性（HCHWA-D）的患者会产生野生型β-淀粉样蛋白（Abetawt）和E22Q突变型β-淀粉样蛋白（AbetaDutch）。对HCHWA-D患者大脑进行的尸检分析显示，存在严重的脑淀粉样血管病，而实质淀粉样蛋白沉积很少。为了研究在同时存在Abetawt和AbetaDutch变体的情况下的淀粉样变性，将转基因（tg）APP23小鼠与APPDutch小鼠进行杂交。尽管单转基因APP23小鼠随着年龄增长会沉积Abetawt，但双转基因APP23/APPDutch小鼠会共同沉积AbetaDutch（主要是AbetaDutch1-40）和Abetawt，总Abeta水平高出两倍。与APP23小鼠相比，APP23/APPDutch小鼠的血管Abeta沉积和出血高出两倍。令人惊讶的是，与单转基因APP23小鼠相比，双转基因小鼠的实质Abeta沉积减少。我们的研究结果表明，AbetaDutch1-40抑制实质淀粉样变性，但会加剧血管淀粉样变性，从而解释了HCHWA-D患者脑淀粉样蛋白在不同区域的特异性分布。