Parallel Mechanisms between Placental Amyloidosis/Preeclampsia and Neurodegenerative Diseases

Abstract

This short review summarizes recent studies on placenta-preeclampsia in the mother and/or intrauterine growth restriction in the child. The ideas raised here are framed within a paradigm that favors the opening of new research lines in these themes and are focused on the outlining of early investigation and/or an adequate treatment for mothers who develop the pathology. Thus, this review focuses on those studies that categorize PE in the group of pathologies defined as "conformational diseases", as a consequence of the misfolding of proteins due to endoplasmic reticulum ER stress. In this particular case, the ER stress that develops in the syncytiotrophoblast because of the oxidative stress caused in the placenta by the hypoxia that occurs as a consequence of the failure in the remodeling of endometrial arteries. This leads to an increased syncytiotrophoblast apoptosis with detachment of misfolded proteins into the maternal circulation, which in turn would be primarily responsible for the signs of preeclampsia in the mother: proteinuria, edema, and hypertension.  The review also analyzes the preeclampsia-prions-placenta relationship, since the normal cell-surface protein PrPc is normally present in the plasma membrane of syncytiotrophoblast, but appears to be increased in cases of preeclampsia. However, although neurodegenerative disorders resulting from conformational changes in the prion protein from its normal cellular form, PrPc, to the infectious scrapie isoform, PrPSc are well known, limited information is available on Pr Pc and PrPSc in the ST, hence review on these proteins gains more attention in normal and pathological placenta.