Characteristic developmental expression of amyloid β40, 42 and 43 in patients with Down syndrome
Characteristic developmental expression of amyloid β40, 42 and 43 in patients with Down syndrome
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DOI：
10.1016/s0387-7604(02)00209-7
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发表时间：
2003-04-01
影响因子：
1.7
通讯作者：
Takashima, S
中科院分区：
文献类型：
--
作者：
Hirayama, A;Horikoshi, Y;Takashima, S
我们采用免疫组织化学方法研究了20例唐氏综合征（DS）患者和13例对照者额叶中β-淀粉样前体蛋白（APP）、A β 40、A β 42和A β 43的表达。每种抗体的免疫反应性在强度程度和表达的时间模式上是不同的。APP和A β 43免疫反应最初在神经元中增加，然后从32岁开始在弥漫性斑块中出现A β 43和A β 42免疫反应。在老年斑周围的轴突中观察到APP和Abeta 43的特征。最后，在老年斑的核心中检测到A β 40免疫反应性。这种免疫反应性表达的时程可能与DS中Alzheimer型痴呆的发病过程有关，老年斑中的轴突损伤可能通过轴突流动障碍和A β 43在皮层神经元中的积聚导致神经元缠结（NFT）的形成或神经元死亡。(C)2002 Elsevier Science B. V.保留所有权利。
We immunohistochemically studied the expression of beta-amyloid precursor protein (APP), Abeta40, Abeta42, and Abeta43 in the frontal lobes of 20 Down syndrome (DS) patients and 13 controls. The immunoreactivity for each antibody was different in the degree of intensity and the chronological pattern of expression. APP and Abeta43 immunoreactivity was increased in neurons initially, and then Abeta43 and 42 immunoreactivity appeared in diffuse plaques from 32 years of age. APP and Abeta43 were characteristically observed in axons around senile plaques. Finally, Abeta40 immunoreactivity was detected in the cores of senile plaques. This time course of immunoreactive expression may be related to the pathogenetic process of Alzheimer-type dementia in DS, and the axonal damage in senile plaques may lead to the formation of neurofibrillary tangles (NFT) or neuronal death through axonal flow disturbance and accumulation of Abeta43 in cortical neurons. (C) 2002 Elsevier Science B.V. All rights reserved.