Amyloid β Protein (Aβ) Starts to Deposit As Plasma Membrane‐Bound Form in Diffuse Plaques of Brains from Hereditary Cerebral Hemorrhage with Amyloidosis‐Dutch Type, Alzheimer Disease and Nondemented Aged Subjects
Amyloid β Protein (Aβ) Starts to Deposit As Plasma Membrane‐Bound Form in Diffuse Plaques of Brains from Hereditary Cerebral Hemorrhage with Amyloidosis‐Dutch Type, Alzheimer Disease and Nondemented Aged Subjects
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β 淀粉样蛋白 (Aβ) 开始以质膜结合形式沉积在患有淀粉样变性荷兰型遗传性脑出血、阿尔茨海默病和非痴呆老年受试者的大脑弥漫斑块中
DOI：
10.1093/jnen/59.8.723
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
R. Roos
中科院分区：
文献类型：
--
作者：
H. Yamaguchi;M. Maat‐Schieman;S. V. van Duinen;F. Prins;Peter Neeskens;R. Roos
为了阐明β-淀粉样蛋白在老年斑中开始存款的位置和方式，我们检测了淀粉样β蛋白（Aβ）在遗传性脑出血伴淀粉样变性-荷兰型、阿尔茨海默病（AD）和非痴呆老年受试者脑弥漫斑中的超微结构定位。用免疫胶体金标记Aβx-42（Aβ42），在透射电镜下观察弥散斑的位置，并在透射电镜下观察。电镜下所有受试者的Aβ42沉积均以3种形式出现：1）细胞突起间散在的小束淀粉样纤维，常见于弥漫性斑块的染色密集区; 2)在细胞突起之间散在的非纤维状物质的小病灶，为相对较小的形式。3)Aβ42位于正常外观细胞突起的细胞表面质膜的一部分上，是弱免疫染色区域的主要形式。最后一种形式与退行性神经突或反应性胶质细胞无关。Aβ42在细胞表面质膜上的沉积似乎是弥漫性斑块中的初始事件，然后在细胞突起之间发展为无定形/纤维状淀粉样蛋白。
To clarify where and how β-amyloid begins to deposit in senile plaques, we examined the ultrastructural localization of amyloid β protein (Aβ) in diffuse plaques of brains with hereditary cerebral hemorrhage with amyloidosis-Dutch type, Alzheimer disease (AD), and from nondemented aged subjects. Serial ultrathin sections of osmium-plastic blocks were immunogold-labeled for Aβx-42 (Aβ42), and sections on grids were observed under the electron microscope (EM) after observing the exact localization of the diffuse plaques in sections on glass slides by the reflection contrast microscope. Aβ42 deposition, which was decollated with gold particles, appeared in 3 forms in all subjects under the EM: 1) Scattered small bundles of amyloid fibrils between cell processes, frequently seen in the densely stained area of diffuse plaques. 2) Scattered small foci of nonfibrillar materials between cell processes as a relatively minor form. 3) Aβ42 on a part of the cell surface plasma membrane of normal appearing cell processes, a major form in weakly immunostained areas. The last form was not associated with degenerative neurites or reactive glia. Aβ42 deposition on the cell surface plasma membrane appears to be an initial event in diffuse plaques, and then it develops into amorphous/fibrillar amyloid between cell processes.
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影响因子：
82.9
作者：
S. J. Lee;U. Liyanage;P. Bickel;W. Xia;P. Lansbury;K. Kosik
通讯作者：
S. J. Lee;U. Liyanage;P. Bickel;W. Xia;P. Lansbury;K. Kosik
DOI：
10.1073/pnas.89.16.7437
发表时间：
1992-08-15
影响因子：
11.1
作者：
KNAUER, MF;SOREGHAN, B;GLABE, CG
通讯作者：
GLABE, CG
DOI：
10.1016/s0021-9258(18)53661-9
发表时间：
1993-02
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
A. Roher;J. Lowenson;S. Clarke;C. Wolkow;Rong Wang;R. Cotter;I. Reardon;H. Zurcher-Neely;R. Heinrikson;M. Ball
通讯作者：
A. Roher;J. Lowenson;S. Clarke;C. Wolkow;Rong Wang;R. Cotter;I. Reardon;H. Zurcher-Neely;R. Heinrikson;M. Ball
影响因子：
56.9
作者：
E. Levy;M. Carman;I. Fernandez‐Madrid;M. Power;I. Lieberburg;S. V. van Duinen;G. Bots;W. Luyendijk;B. Frangione
通讯作者：
E. Levy;M. Carman;I. Fernandez‐Madrid;M. Power;I. Lieberburg;S. V. van Duinen;G. Bots;W. Luyendijk;B. Frangione
影响因子：
2.9
作者：
JARRETT, JT;BERGER, EP;LANSBURY, PT
通讯作者：
LANSBURY, PT