<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Wisch JK</submitter><funding>NIA NIH HHS</funding><pubmed_abstract>Down syndrome is characterized by triplication of chromosome 21, leading to early-onset Alzheimer disease pathology, with nearly all individuals with Down syndrome developing amyloid and tau pathology. In the new era of amyloid modifying therapies, it is vital to identify early biomarkers for Alzheimer disease (AD) pathology in Down syndrome. Striatal amyloid may begin to accumulate sooner than cortical amyloid in Down syndrome. Tau phosphorylation at specific sites, including 217, can be quantified in plasma and may represent an important mechanistic step in the development of tau pathology. This study had two aims: 1. To compare the relative age at increase of multiple biomarkers (cortical amyloid, striatal amyloid, plasma pTau217 and summary tau pathology) 2. To test whether plasma pTau</pubmed_abstract><journal>Brain : a journal of neurology</journal><pagination>awaf418</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12917769</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Imaging and plasma biomarkers for pathological accumulation in Down syndrome.</pubmed_title><pmcid>PMC12917769</pmcid><funding_grant_id>U01 AG051412</funding_grant_id><funding_grant_id>U01 AG051406</funding_grant_id><funding_grant_id>U19 AG068054</funding_grant_id><pubmed_authors>Petersen M</pubmed_authors><pubmed_authors>Schlachetzki Z</pubmed_authors><pubmed_authors>Zaman S</pubmed_authors><pubmed_authors>Lai F</pubmed_authors><pubmed_authors>Tudorascu D</pubmed_authors><pubmed_authors>Rosas HD</pubmed_authors><pubmed_authors>Ances BM</pubmed_authors><pubmed_authors>Schmitt FA</pubmed_authors><pubmed_authors>Lott IT</pubmed_authors><pubmed_authors>Handen BL</pubmed_authors><pubmed_authors>Ibanez L</pubmed_authors><pubmed_authors>Lee JH</pubmed_authors><pubmed_authors>Mapstone M</pubmed_authors><pubmed_authors>Cohen AD</pubmed_authors><pubmed_authors>Hom C</pubmed_authors><pubmed_authors>Christian BT</pubmed_authors><pubmed_authors>Krinsky-McHale SJ</pubmed_authors><pubmed_authors>Ptomey L</pubmed_authors><pubmed_authors>Rafii MS</pubmed_authors><pubmed_authors>Kennedy JT</pubmed_authors><pubmed_authors>Burns JM</pubmed_authors><pubmed_authors>Wisch JK</pubmed_authors><pubmed_authors>Harp JP</pubmed_authors><pubmed_authors>Hartley S</pubmed_authors><pubmed_authors>Jiao Z</pubmed_authors><pubmed_authors>Head E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Imaging and plasma biomarkers for pathological accumulation in Down syndrome.</name><description>Down syndrome is characterized by triplication of chromosome 21, leading to early-onset Alzheimer disease pathology, with nearly all individuals with Down syndrome developing amyloid and tau pathology. In the new era of amyloid modifying therapies, it is vital to identify early biomarkers for Alzheimer disease (AD) pathology in Down syndrome. Striatal amyloid may begin to accumulate sooner than cortical amyloid in Down syndrome. Tau phosphorylation at specific sites, including 217, can be quantified in plasma and may represent an important mechanistic step in the development of tau pathology. This study had two aims: 1. To compare the relative age at increase of multiple biomarkers (cortical amyloid, striatal amyloid, plasma pTau217 and summary tau pathology) 2. To test whether plasma pTau</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Nov</publication><modification>2026-07-16T09:44:51.924Z</modification><creation>2026-07-09T10:47:19.193Z</creation></dates><accession>S-EPMC12917769</accession><cross_references><pubmed>41205623</pubmed><doi>10.1093/brain/awaf418</doi></cross_references></HashMap>