<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Eid A</submitter><funding>NIA NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>87005</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9364816</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>130(8)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The interaction of aging-related, genetic, and environmental factors is thought to contribute to the etiology of late-onset, sporadic Alzheimer's disease (AD). We previously reported that serum levels of &lt;i>p,p&lt;/i>'-dichlorodiphenyldichloroethylene (DDE), a long-lasting metabolite of the organochlorine pesticide dichlorodiphenyltrichloroethane (DDT), were significantly elevated in patients with AD and associated with the risk of AD diagnosis. However, the mechanism by which DDT may contribute to AD pathogenesis is unknown.&lt;h4>Objectives&lt;/h4>This study sought to assess effects of DDT exposure on the amyloid pathway in multiple &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i> models.&lt;h4>Methods&lt;/h4>Cultured cells (SH-SY5Y and primary neurons), transgenic flies overexpressing amyloid bet</pubmed_abstract><journal>Environmental health perspectives</journal><pubmed_title>Effects of DDT on Amyloid Precursor Protein Levels and Amyloid Beta Pathology: Mechanistic Links to Alzheimer's Disease Risk.</pubmed_title><pmcid>PMC9364816</pmcid><funding_grant_id>R01 ES026057</funding_grant_id><funding_grant_id>R13 AG069380</funding_grant_id><funding_grant_id>R01 ES024288</funding_grant_id><funding_grant_id>U01 NS108956</funding_grant_id><funding_grant_id>R01 ES027481</funding_grant_id><funding_grant_id>P30 ES005022</funding_grant_id><funding_grant_id>R01 ES021800</funding_grant_id><pubmed_authors>Mhatre-Winters I</pubmed_authors><pubmed_authors>Lisci M</pubmed_authors><pubmed_authors>Hart RP</pubmed_authors><pubmed_authors>Bennett JW</pubmed_authors><pubmed_authors>Hossain MM</pubmed_authors><pubmed_authors>Richardson JR</pubmed_authors><pubmed_authors>Carney K</pubmed_authors><pubmed_authors>Konsolaki M</pubmed_authors><pubmed_authors>Han Y</pubmed_authors><pubmed_authors>Edler MK</pubmed_authors><pubmed_authors>Sammoura FM</pubmed_authors><pubmed_authors>von Stein R</pubmed_authors><pubmed_authors>Eid A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Effects of DDT on Amyloid Precursor Protein Levels and Amyloid Beta Pathology: Mechanistic Links to Alzheimer's Disease Risk.</name><description>&lt;h4>Background&lt;/h4>The interaction of aging-related, genetic, and environmental factors is thought to contribute to the etiology of late-onset, sporadic Alzheimer's disease (AD). We previously reported that serum levels of &lt;i>p,p&lt;/i>'-dichlorodiphenyldichloroethylene (DDE), a long-lasting metabolite of the organochlorine pesticide dichlorodiphenyltrichloroethane (DDT), were significantly elevated in patients with AD and associated with the risk of AD diagnosis. However, the mechanism by which DDT may contribute to AD pathogenesis is unknown.&lt;h4>Objectives&lt;/h4>This study sought to assess effects of DDT exposure on the amyloid pathway in multiple &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i> models.&lt;h4>Methods&lt;/h4>Cultured cells (SH-SY5Y and primary neurons), transgenic flies overexpressing amyloid bet</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2025-04-04T10:44:37.065Z</modification><creation>2025-04-04T10:44:37.065Z</creation></dates><accession>S-EPMC9364816</accession><cross_references><pubmed>35946953</pubmed><doi>10.1289/EHP10576</doi></cross_references></HashMap>