<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Barry A</submitter><funding>National Center for Advancing Translational Sciences</funding><funding>NCATS NIH HHS</funding><funding>NICHD NIH HHS</funding><funding>NIA NIH HHS</funding><funding>Alzheimer's Disease Research Centers Program</funding><funding>National Centralized Repository for Alzheimer Disease and Related Dementias</funding><funding>National Institute on Aging and the National Institute for Child Health and Human Development</funding><funding>DS-Connect</funding><pagination>e70211</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12035545</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(4)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Gait abnormalities are associated with Alzheimer's disease (AD) in the general population, but it is unclear if the same is true for individuals with Down syndrome (DS). This study examined gait across 32 months in relation to neuroimaging biomarkers (amyloid beta [Aβ], neurofibrillary tangles [NFTs], and hippocampal volume), cognitive decline, and clinical AD status in adults with DS.&lt;h4>Methods&lt;/h4>Participants were 218 adults with DS who underwent Aβ and NFT positron emission tomography (PET) and magnetic resonance imaging (MRI) scans, cognitive testing, and gait assessments at baseline and 32 months. Residual change regression models were conducted.&lt;h4>Results&lt;/h4>Higher baseline Aβ PET and NFT PET and lower MRI hippocampal volume were associated with gait declines</pubmed_abstract><journal>Alzheimer's &amp; dementia : the journal of the Alzheimer's Association</journal><pubmed_title>Longitudinal investigation of gait and Alzheimer's disease in adults with Down syndrome.</pubmed_title><pmcid>PMC12035545</pmcid><funding_grant_id>U24 AG21886</funding_grant_id><funding_grant_id>P50 AG008702</funding_grant_id><funding_grant_id>UL1 TR002373</funding_grant_id><funding_grant_id>UL1 TR001873</funding_grant_id><funding_grant_id>UL1 TR002345</funding_grant_id><funding_grant_id>P30 AG062421</funding_grant_id><funding_grant_id>U54 HD087011</funding_grant_id><funding_grant_id>UL1 TR001414</funding_grant_id><funding_grant_id>P50 AG005681</funding_grant_id><funding_grant_id>P50 HD105353</funding_grant_id><funding_grant_id>U19 AG068054</funding_grant_id><funding_grant_id>P50 AG005133</funding_grant_id><funding_grant_id>UL1 TR001857</funding_grant_id><funding_grant_id>P30 AG062715</funding_grant_id><funding_grant_id>P30 AG066519</funding_grant_id><funding_grant_id>U01 AG051412</funding_grant_id><funding_grant_id>U01 AG051406</funding_grant_id><funding_grant_id>P50 AG16537</funding_grant_id><funding_grant_id>U54 HD090256</funding_grant_id><funding_grant_id>RO1 AG070028</funding_grant_id><pubmed_authors>Barry A</pubmed_authors><pubmed_authors>Lai F</pubmed_authors><pubmed_authors>Hom CL</pubmed_authors><pubmed_authors>Minhas D</pubmed_authors><pubmed_authors>Ances BM</pubmed_authors><pubmed_authors>Alzheimer Biomarker Consortium ‐ Down syndrome</pubmed_authors><pubmed_authors>Zaman SH</pubmed_authors><pubmed_authors>Lott I</pubmed_authors><pubmed_authors>Handen BL</pubmed_authors><pubmed_authors>Lee JH</pubmed_authors><pubmed_authors>Mapstone M</pubmed_authors><pubmed_authors>Price J</pubmed_authors><pubmed_authors>Christian BT</pubmed_authors><pubmed_authors>Krinsky-McHale SJ</pubmed_authors><pubmed_authors>Glueck A</pubmed_authors><pubmed_authors>Harp J</pubmed_authors><pubmed_authors>Zammit M</pubmed_authors><pubmed_authors>Laymon C</pubmed_authors><pubmed_authors>Schmitt F</pubmed_authors><pubmed_authors>Clare ICH</pubmed_authors><pubmed_authors>Cohen A</pubmed_authors><pubmed_authors>Hartley SL</pubmed_authors><pubmed_authors>Bolt D</pubmed_authors><pubmed_authors>Luo W</pubmed_authors><pubmed_authors>Rosa HD</pubmed_authors><pubmed_authors>Pulsifer M</pubmed_authors><pubmed_authors>Head E</pubmed_authors><pubmed_authors>Peven JC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Longitudinal investigation of gait and Alzheimer's disease in adults with Down syndrome.</name><description>&lt;h4>Introduction&lt;/h4>Gait abnormalities are associated with Alzheimer's disease (AD) in the general population, but it is unclear if the same is true for individuals with Down syndrome (DS). This study examined gait across 32 months in relation to neuroimaging biomarkers (amyloid beta [Aβ], neurofibrillary tangles [NFTs], and hippocampal volume), cognitive decline, and clinical AD status in adults with DS.&lt;h4>Methods&lt;/h4>Participants were 218 adults with DS who underwent Aβ and NFT positron emission tomography (PET) and magnetic resonance imaging (MRI) scans, cognitive testing, and gait assessments at baseline and 32 months. Residual change regression models were conducted.&lt;h4>Results&lt;/h4>Higher baseline Aβ PET and NFT PET and lower MRI hippocampal volume were associated with gait declines</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2025-07-11T03:03:48.962Z</modification><creation>2025-07-11T03:03:48.962Z</creation></dates><accession>S-EPMC12035545</accession><cross_references><pubmed>40289844</pubmed><doi>10.1002/alz.70211</doi></cross_references></HashMap>