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Plasma amyloid beta protein 1-42 levels in fetuses with Down syndrome
Jose L Bartha1, Peter W Soothill
1Fetal Medicine Research Unit, Department of Obstetrics and Gynaecology, St Michael's Hospital, University of Bristol, Bristol, UK. joseluis.bartha@uca.es
Background:
The presence of amyloid plaques in the brains of people with Down syndrome is correlated with the severity and the progression of the disease. The core of the plaques is an amyloid beta (A beta) protein. If a relationship between fetal levels and the presence and severity of the disease could be determined, consideration of an early intervention to reduce brain damage can be proposed.
Aim:
To study plasma amyloid beta 1-42 levels in fetuses with Down syndrome.
Study Design:
Fetal plasma amyloid beta 1-42 levels were measured using a commercially available immunoassay. The sample size was previously calculated to show a difference with an alpha level of 0.05 and a power (1-beta) of 90%.
Subjects:
Thirteen fetuses with Down syndrome and 17 controls (22.3+/-2.0 and 21.6+/-1.2 weeks of gestation, respectively).
Outcome Measures:
Fetal plasma amyloid beta 1-42 levels.
Results:
There was no significant difference in plasma amyloid beta 1-42 levels between fetuses with Down syndrome and those with a normal karyotype (193.1+/-48.0 vs. 194.6+/-15.6 pg/mL, respectively).
Conclusions:
This result does not support the hypothesis that A beta 1-42 may be related to the severity of brain damage in newborns with Down syndrome. The high levels of this peptide in fetuses without Down syndrome favour a physiological role of these peptides during brain development.
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