Comparison of Abeta levels in the brain of familial and sporadic Alzheimer's disease.
Comparison of Abeta levels in the brain of familial and sporadic Alzheimer's disease.
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DOI：
10.1016/j.neuint.2009.03.007
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发表时间：
2009-09
影响因子：
4.2
通讯作者：
Marutle A
中科院分区：
文献类型：
--
作者：
Hellström-Lindahl E;Viitanen M;Marutle A
早老素（PS）和淀粉样前体蛋白（APP）基因突变是早发性家族性阿尔茨海默病（AD）的主要病因。我们测量了APPsw和PS1（M146 V）突变携带者、散发性AD（SAD）和非痴呆个体皮质中的Aβ水平。APPsw突变携带者脑内不溶性和可溶性Aβ40及可溶性Aβ42水平与SAD患者无明显差异，但APPsw突变携带者脑内额叶和颞叶皮质内不溶性Aβ42水平较低。与SAD组相比，PS1组所有4个皮质区的不溶性Aβ40和Aβ42均显著降低，与APPsw组相比，额叶和枕叶皮质的Aβ40均显著降低。SAD和APPsw患者的不溶性Aβ42/40比值相似，但PS1突变携带者的不溶性Aβ42/40比值显著较高。我们的结果表明，PS1突变携带者的Aβ沉积模式与APPsw和SAD不同，而APPsw突变携带者的A β沉积模式与SAD更相似。PS1 AD的早发和侵袭性病程不能仅用Aβ水平升高来解释，至少在本文研究的PS1 M146 V突变携带者中是如此。
Mutations in presenilin (PS) and amyloid precursor protein (APP) genes are a major cause for early-onset familial Alzheimer disease (AD). We measured Aβ levels in the cortex of APPsw and PS1 (M146V) mutation carriers, sporadic AD (SAD) and non-demented individuals. Levels of insoluble and soluble Aβ40 and soluble Aβ42 in brain of APPsw mutation carriers did not differ much from those found in SAD, but lower levels of insoluble Aβ42 were detected in the frontal and temporal cortex of APPsw brain. Insoluble Aβ40 and Aβ42 were significant lower in all four cortical regions of PS1 brain compared with SAD, and Aβ40 was lower in frontal and occipital cortex compared with APPsw brain. The insoluble Aβ42/40 ratio was similar in SAD and APPsw but significantly higher in PS1 mutation carriers. Our results indicate that the pattern of Aβ deposition in PS1 mutation carriers differs from that in both APPsw and SAD, whereas the pattern in APPsw mutation carriers is more similar to that in SAD. The early onset and aggressive course of PS1 AD cannot solely be explained by elevated Aβ levels, at least in the PS1 M146V mutation carries investigated here.
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