2019
DOI: 10.1080/01443615.2019.1679734
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Comparison of serum human pregnancy-specific beta-1-glycoprotein 1 levels in pregnant women with or without preeclampsia

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Cited by 18 publications
(10 citation statements)
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“…The protective haplotype also lies within a large cluster of PSG genes, a family of glycoproteins that are primarily synthesized in the syncytiotrophoblast of the human placenta. Several case-control studies have shown that low levels of PSG2 are associated with pre-eclampsia [21], which, in turn, has been suggested to be associated with an increased risk of dementia later in life [22]. Indeed, a recent study demonstrated that inducible pluripotent stem cell (iPSC) derived neurons made from the blood of autopsy confirmed AD patients, had abnormal tau deposition which matched their autopsy findings [23].…”
Section: Plos Geneticsmentioning
confidence: 99%
“…The protective haplotype also lies within a large cluster of PSG genes, a family of glycoproteins that are primarily synthesized in the syncytiotrophoblast of the human placenta. Several case-control studies have shown that low levels of PSG2 are associated with pre-eclampsia [21], which, in turn, has been suggested to be associated with an increased risk of dementia later in life [22]. Indeed, a recent study demonstrated that inducible pluripotent stem cell (iPSC) derived neurons made from the blood of autopsy confirmed AD patients, had abnormal tau deposition which matched their autopsy findings [23].…”
Section: Plos Geneticsmentioning
confidence: 99%
“…Several studies have reported that expression of CGB5 was essential for pregnancy success [30]. Aberrations of CRH (corticotropin releasing hormone) [31] and PSG1 [32] contribute to preeclampsia occurrence. The expression of CYP19A1 was significantly up regulated in hypertensive disorders of pregnancy [33].…”
Section: Discussionmentioning
confidence: 99%
“…It is also associated with significant fetal morbidity and mortality, including intrauterine growth restriction, placental abruption, oligohydramnios, stillbirth, and fetal death ( 4 , 5 ). The exact etiology of PE remains unclear ( 4 ), but hypotheses include abnormal placental implantation ( 4 ), angiogenic pathways ( 4 , 9 , 10 ), cardiovascular maladaptation and vasoconstriction ( 4 ), genetic predisposition ( 4 ), immunology ( 4 ), oxidative stress ( 4 , 5 , 11 ), autocrine/paracrine factors ( 12 , 13 ), and capillary rarefaction ( 14 ). Clinical practice guidelines strongly recommend low-dose aspirin at 12–16 weeks’ gestation for pregnant women at high risk of PE ( 15 , 16 ).…”
Section: Introductionmentioning
confidence: 99%