Prenatal Lead Levels, Plasma Amyloid β Levels, and Gene Expression in Young Adulthood
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Prenatal Lead Levels, Plasma Amyloid β Levels, and Gene Expression in Young Adulthood
| Title: | Prenatal Lead Levels, Plasma Amyloid β Levels, and Gene Expression in Young Adulthood |
| Author: |
Mazumdar, Maitreyi; Xia, Weiming; Sui, Shannan Ho; Needleman, Herbert L.; Hofmann, Oliver Marc; Gregas, Matthew; Hide, Winston; Yang, Ting; Bellinger, David C.
Note: Order does not necessarily reflect citation order of authors. |
| Citation: | Mazumdar, Maitreyi, Weiming Xia, Oliver Hofmann, Matthew Gregas, Shannan Ho Sui, Winston Hide, Ting Yang, Herbert L. Needleman, and David C. Bellinger. 2012. Prenatal lead levels, plasma amyloid β levels, and gene expression in young adulthood. Environmental Health Perspectives 120(5): 702-707. |
| Full Text & Related Files: |
3346789.pdf (339.8Kb; PDF) 
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| Abstract: | Background: Animal studies suggest that early-life lead exposure influences gene expression and production of proteins associated with Alzheimer’s disease (AD). Objectives: We attempted to assess the relationship between early-life lead exposure and potential biomarkers for AD among young men and women. We also attempted to assess whether early-life lead exposure was associated with changes in expression of AD-related genes. Methods: We used sandwich enzyme-linked immunosorbent assays (ELISA) to measure plasma concentrations of amyloid β proteins Aβ40 and Aβ42 among 55 adults who had participated as newborns and young children in a prospective cohort study of the effects of lead exposure on development. We used RNA microarray techniques to analyze gene expression. Results: Mean plasma Aβ:42 concentrations were lower among 13 participants with high umbilical cord blood lead concentrations (≥ 10 μg/dL) than in 42 participants with lower cord blood lead concentrations (p = 0.08). Among 10 participants with high prenatal lead exposure, we found evidence of an inverse relationship between umbilical cord lead concentration and expression of ADAM metallopeptidase domain 9 (ADAM9), reticulon 4 (RTN4), and low-density lipoprotein receptor-related protein associated protein 1 (LRPAP1) genes, whose products are believed to affect Aβ production and deposition. Gene network analysis suggested enrichment in gene sets involved in nerve growth and general cell development. Conclusions: Data from our exploratory study suggest that prenatal lead exposure may influence Aβ-related biological pathways that have been implicated in AD onset. Gene network analysis identified further candidates to study the mechanisms of developmental lead neurotoxicity. |
| Published Version: | doi:10.1289/ehp.1104474 |
| Other Sources: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3346789/pdf/ |
| Terms of Use: | This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA |
| Citable link to this page: | http://nrs.harvard.edu/urn-3:HUL.InstRepos:10483979 |
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