Show simple item record

dc.contributor.authorMazumdar, Maitreyi
dc.contributor.authorXia, Weiming
dc.contributor.authorHofmann, Oliver Marc
dc.contributor.authorGregas, Matthew
dc.contributor.authorSui, Shannan Ho
dc.contributor.authorHide, Winston
dc.contributor.authorYang, Ting
dc.contributor.authorNeedleman, Herbert L.
dc.contributor.authorBellinger, David C.
dc.date.accessioned2013-04-01T19:10:09Z
dc.date.issued2012
dc.identifier.citationMazumdar, 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.en_US
dc.identifier.issn0091-6765en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10483979
dc.description.abstractBackground: 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.en_US
dc.language.isoen_USen_US
dc.publisherNational Institute of Environmental Health Sciencesen_US
dc.relation.isversionofdoi:10.1289/ehp.1104474en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3346789/pdf/en_US
dash.licenseLAA
dc.titlePrenatal Lead Levels, Plasma Amyloid β Levels, and Gene Expression in Young Adulthooden_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalEnvironmental Health Perspectivesen_US
dash.depositing.authorHide, Winston
dc.date.available2013-04-01T19:10:09Z
dc.identifier.doi10.1289/ehp.1104474*
dash.contributor.affiliatedYang, Ting
dash.contributor.affiliatedHofmann, Oliver
dash.contributor.affiliatedHide, Winston
dash.contributor.affiliatedBellinger, David


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record