<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tosun D</submitter><funding>NIH/NIA</funding><funding>National Institute of Neurological Disorders and Stroke</funding><funding>NIA NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>5114-5131</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11350010</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(8)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed.&lt;h4>Methods&lt;/h4>A validated α-synuclein Seed Amplification Assay (SAA) was used on recent cerebrospinal fluid (CSF) samples from 1638 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants, 78 with LB-pathology confirmation at autopsy. We compared SAA outcomes with neuropathology, Aβ and tau biomarkers, risk-factors, genetics, and cognitive trajectories.&lt;h4>Results&lt;/h4>SAA showed 79% sensitivity and 97% specificity for LB pathology, with superior performance in identifying neocortical (100%) compared to limbic (57%) and amygdala-predominant (60%) LB-pa</pubmed_abstract><journal>Alzheimer's &amp; dementia : the journal of the Alzheimer's Association</journal><pubmed_title>A cross-sectional study of α-synuclein seed amplification assay in Alzheimer's disease neuroimaging initiative: Prevalence and associations with Alzheimer's disease biomarkers and cognitive function.</pubmed_title><pmcid>PMC11350010</pmcid><funding_grant_id>U19 AG024904</funding_grant_id><funding_grant_id>AG000546</funding_grant_id><funding_grant_id>U01 AG024904</funding_grant_id><pubmed_authors>Saykin AJ</pubmed_authors><pubmed_authors>Singleton AB</pubmed_authors><pubmed_authors>Thropp P</pubmed_authors><pubmed_authors>MacLeod K</pubmed_authors><pubmed_authors>Blauwendraat C</pubmed_authors><pubmed_authors>McEvoy S</pubmed_authors><pubmed_authors>Alzheimer's Disease Neuroimaging Initiative</pubmed_authors><pubmed_authors>Tosun D</pubmed_authors><pubmed_authors>Hausle Z</pubmed_authors><pubmed_authors>Weiner MW</pubmed_authors><pubmed_authors>Lamoureux J</pubmed_authors><pubmed_authors>Iwaki H</pubmed_authors><pubmed_authors>Lee EB</pubmed_authors><pubmed_authors>Perrin RJ</pubmed_authors><pubmed_authors>Shaw LM</pubmed_authors><pubmed_authors>Nalls M</pubmed_authors><pubmed_authors>Lebovitz R</pubmed_authors></additional><is_claimable>false</is_claimable><name>A cross-sectional study of α-synuclein seed amplification assay in Alzheimer's disease neuroimaging initiative: Prevalence and associations with Alzheimer's disease biomarkers and cognitive function.</name><description>&lt;h4>Introduction&lt;/h4>Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed.&lt;h4>Methods&lt;/h4>A validated α-synuclein Seed Amplification Assay (SAA) was used on recent cerebrospinal fluid (CSF) samples from 1638 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants, 78 with LB-pathology confirmation at autopsy. We compared SAA outcomes with neuropathology, Aβ and tau biomarkers, risk-factors, genetics, and cognitive trajectories.&lt;h4>Results&lt;/h4>SAA showed 79% sensitivity and 97% specificity for LB pathology, with superior performance in identifying neocortical (100%) compared to limbic (57%) and amygdala-predominant (60%) LB-pa</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2025-04-19T01:43:33.35Z</modification><creation>2025-04-19T01:43:33.35Z</creation></dates><accession>S-EPMC11350010</accession><cross_references><pubmed>38770829</pubmed><doi>10.1002/alz.13858</doi></cross_references></HashMap>