Prenatal mercury exposure, neurodevelopment and apolipoprotein E genetic polymorphism

Abstract

The aim of the present study was to evaluate the association between prenatal exposure to mercury (Hg) and neurodevelopment of the child, taking into account genetic polymorphism of apolipoprotein E (Apoe) and other relevant confounders. Six hundred and one mother-child pairs were recruited from the central Slovenia region and 243 from Rijeka, on the Croatian coast of the northern Adriatic. The total Hg in cord blood, Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III) assessment at 18 months of age and Apoe genotyping was performed on 361 children; 237 of them were from Slovenia and 124 from Croatia. The results showed negative association between low-to-moderate Hg exposure in children with normal neurodevelopmental outcome and cognitive and fine motor scores at 18 months of age as assessed by Bayley III. The Hg-related decrease in cognitive score was observed only in children carrying at least one Apoe ε4 allele, while the decrease in fine motor scores was independent of the Apoe genotype. Adjusting for selenium (Se) and lead (Pb) levels, a positive association between Se and the language score and a negative association between Pb and the motor score was observed, but not in the subgroup of children carrying the ε4 allele.

Maternal selenium status and neuropsychological development in Spanish preschool children

“…(Skröder et al, 2015) and Poland (mean of Se in serum at the first trimester of pregnancy: 48.3 µg/L) (Polanska et al, 2016(Polanska et al, , 2017. Additionally, a positive, but only marginally significant, association was observed between cord blood Se serum (geometric mean of 40.1 ng/g) and the language domain among children who were non-carriers of the ε4 allele for the apolipoprotein E gene, but not in the ε4 carriers (Snoj Tratnik et al, 2017). This ε4 allele was also found to be a modifier of the association between mercury and cognitive performance in the same population, the carrier children being the ones who obtained poorer scores.…”

Mercury and Alzheimer’s Disease: Hg(II) Ions Display Specific Binding to the Amyloid-β Peptide and Hinder Its Fibrillization

“…Interestingly, AD and Hg intoxication have a common risk factor in the gene encoding the apolipoprotein E (ApoE). Hg exposure typically produces worse outcomes in individuals with the ApoEε4 allele [170][171][172][173], and this allele is linked also to an increased probability of developing AD [8][9][10][11]14]. The underlying reasons for this similar risk factor are unclear, however, and a number of explanations have been proposed [8,174], including the possibility that the beneficial ApoE variants may interact with and promote clearance of the Aβ peptide [175] or Hg ions [9,11].…”

Role for apolipoprotein E in neurodegeneration and mercury intoxication

“…Still, this limit is based on acute outbreaks such as those in Minamata and Iraq; some studies have shown in recent years that exposure to relatively low levels of methylmercury (below the WHO limit) have the potential to cause additional long-term consequences such as genotoxicity (9,(23)(24)(25). Although recent studies on AD patients or older individuals have failed to find correlations between the content of mercury and neurodegenerative processes (2,26), chronic neurodegeneration due to chronic methylmercury exposure may be better associated with longitudinal assessments of mercury levels (7,(11)(12)(13)(14)(15)(16).…”