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β-淀粉样蛋白沉积与头部创伤。

Beta AP deposition and head trauma.

作者信息

Adle-Biassette H, Duyckaerts C, Wasowicz M, He Y, Fornes P, Foncin J F, Lecomte D, Hauw J J

机构信息

Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France.

出版信息

Neurobiol Aging. 1996 May-Jun;17(3):415-9. doi: 10.1016/0197-4580(96)00029-2.

DOI:10.1016/0197-4580(96)00029-2
PMID:8725903
Abstract

Head trauma is considered to be a risk factor for Alzheimer's disease, because a high prevalence of beta AP deposits has repeatedly been reported in patients who died within a few days following head injury. To evaluate this statement, we undertook two studies using immunohistochemistry for beta AP and found a surprisingly low prevalence of beta AP diffuse deposits. We first selected 23 patients aged 17-63 years, who died 0-76 days after head trauma. Using beta AP antibody at the usual dilution (1:100), we did not find any deposits. With a high concentration of antibody (dilution 1:2) we found beta AP diffuse deposits in one 46-year-old case. In a second study, 17 patients aged 60-79 years old, who died 1-35 days after head injury, were compared to a control group. We did not find any significant difference in the density of beta AP diffuse deposits between cases and controls using usual dilutions of beta AP antibody. The density of beta AP diffuse deposits was linked only to aging and the presence of senile plaques.

摘要

头部创伤被认为是阿尔茨海默病的一个风险因素,因为在头部受伤后几天内死亡的患者中,β淀粉样蛋白(beta AP)沉积物的高患病率屡有报道。为了评估这一说法,我们进行了两项使用β淀粉样蛋白免疫组织化学的研究,结果发现β淀粉样蛋白弥漫性沉积物的患病率出奇的低。我们首先选择了23名年龄在17至63岁之间的患者,他们在头部创伤后0至76天死亡。使用通常稀释度(1:100)的β淀粉样蛋白抗体,我们未发现任何沉积物。使用高浓度抗体(稀释度1:2)时,我们在一名46岁的病例中发现了β淀粉样蛋白弥漫性沉积物。在第二项研究中,将17名年龄在60至79岁之间、在头部受伤后1至35天死亡的患者与一个对照组进行了比较。使用β淀粉样蛋白抗体的通常稀释度时,我们未发现病例组和对照组之间β淀粉样蛋白弥漫性沉积物密度有任何显著差异。β淀粉样蛋白弥漫性沉积物的密度仅与衰老和老年斑的存在有关。

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Beta AP deposition and head trauma.β-淀粉样蛋白沉积与头部创伤。
Neurobiol Aging. 1996 May-Jun;17(3):415-9. doi: 10.1016/0197-4580(96)00029-2.
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Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease.严重颅脑损伤后脑内β淀粉样蛋白沉积:对阿尔茨海默病发病机制的启示
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J Neurosci Res. 1990 Dec;27(4):587-94. doi: 10.1002/jnr.490270420.
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Amyloid beta-protein ending at Thr43 is a minor component of some diffuse plaques in the Alzheimer's disease brain, but is not found in cerebrovascular amyloid.以苏氨酸43结尾的β淀粉样蛋白是阿尔茨海默病大脑中一些弥漫性斑块的次要成分,但在脑血管淀粉样蛋白中未发现。
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Immunohistological study of senile brains by using a monoclonal antibody recognizing beta amyloid precursor protein: significance of granular deposits in relation with senile plaques.使用识别β淀粉样前体蛋白的单克隆抗体对老年大脑进行免疫组织学研究:颗粒状沉积物与老年斑的关系及意义。
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High sensitivity analysis of amyloid-beta peptide composition in amyloid deposits from human and PS2APP mouse brain.人源和PS2APP小鼠脑内淀粉样沉积物中β淀粉样肽组成的高灵敏度分析
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[Similarities between cerebral amyloid plaques in aged lemurian and in human with Alzheimer's disease].[老年利莫里亚人(传说中的人类群体)与患有阿尔茨海默病的人类大脑中淀粉样斑块的相似性]
C R Seances Soc Biol Fil. 1993;187(4):516-25.
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[Alzheimer's disease: lesions and their progression].[阿尔茨海默病:病变及其进展]
Rev Neurol (Paris). 1999;155 Suppl 4:S17-27.

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Environmental factors in the development and progression of late-onset Alzheimer's disease.迟发性阿尔茨海默病发生与进展中的环境因素
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