High beta-amyloid(1–40) cerebrospinal fluid concentrations precede increase of serum biomarkers in a case with severe HELLP syndrome

IF 3 2区 医学 Q2 DEVELOPMENTAL BIOLOGY
C. Alomar-Dominguez, W. Lederer
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引用次数: 0

Abstract

Beta-amyloid peptides and tau protein concentrations were analysed at second and third trimester pregnancy in cerebrospinal fluid in a 27-year old woman who developed severe HELLP (Hemolysis, Elevated Liver enzymes and Low Platelets) syndrome. Contrary to a healthy pregnant control the beta-amyloid(1–40) load was much higher and the ratios beta-amyloid peptides(1–42/1-40) and phospho-tau/tau had increased before delivery. We observed that in early HELLP syndrome increased beta-amyloid levels preceded vascular biomarker changes. We conclude that high levels of beta-amyloid(1–40) in the second trimester of pregnancy might reflect pathologic maternal brain changes that go along with pathological changes in the materno-feto-placental unit.

Abstract Image

一名重度 HELLP 综合征患者在血清生物标志物增加前脑脊液中的β-淀粉样蛋白(1-40)浓度较高
我们对一名患有严重HELLP(溶血、肝酶升高和血小板降低)综合征的27岁女性在怀孕第二和第三季度脑脊液中的β-淀粉样蛋白肽和tau蛋白浓度进行了分析。与健康孕妇对照组相比,β-淀粉样蛋白(1-40)的含量要高得多,β-淀粉样蛋白肽(1-42/1-40)和磷酸化陶氏肽/陶氏肽的比率在分娩前也有所增加。我们观察到,在早期 HELLP 综合征中,β-淀粉样蛋白水平的增加先于血管生物标志物的变化。我们的结论是,妊娠后三个月的β-淀粉样蛋白(1-40)高水平可能反映了母体脑部的病理变化,这种变化与母胎-胎盘单元的病理变化同时发生。
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来源期刊
Placenta
Placenta 医学-发育生物学
CiteScore
6.30
自引率
10.50%
发文量
391
审稿时长
78 days
期刊介绍: Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.
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