<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee SY</submitter><funding>Alzheimer's Association Research</funding><funding>New Vision Research Charleston Conference on Alzheimer's Disease</funding><funding>NIA)</funding><funding>Larry L. Hillblom Foundation</funding><funding>NIH)</funding><pagination>e70626</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12412752</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(9)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Glial fibrillary acidic protein (GFAP) may contribute to Alzheimer's pathology at early disease stages. GFAP moderation of Alzheimer's disease (AD)-related neurodegeneration and cognition is unclear.&lt;h4>Methods&lt;/h4>We examined plasma GFAP moderation of AD biomarkers (amyloid beta [Aβ]-positron emission tomography [PET][A]; plasma phosphorylated tau-181 [p-tau181][T&lt;sub>1&lt;/sub>]), neurodegeneration (plasma NfL[N&lt;sub>plasma&lt;/sub>]; structural magnetic resonance imaging [MRI][N&lt;sub>MRI&lt;/sub>]), and cognition (Cog&lt;sub>memory&lt;/sub>; Cog&lt;sub>executive&lt;/sub>) in two cohorts: University of California San Francisco (UCSF) (N = 212, 91.0% non-Hispanic/Latino White [NHLW], age = 74.7 [7.6] years, 75.9% cognitively unimpaired [CU]) and 1Florida Alzheimer's Disease Research Centers</pubmed_abstract><journal>Alzheimer's &amp; dementia : the journal of the Alzheimer's Association</journal><pubmed_title>Moderating effects of plasma glial fibrillary acidic protein along the Alzheimer's disease continuum.</pubmed_title><pmcid>PMC12412752</pmcid><funding_grant_id>UF1NS100608</funding_grant_id><funding_grant_id>R01AG032289</funding_grant_id><funding_grant_id>R01AG072475</funding_grant_id><funding_grant_id>K23AG084883</funding_grant_id><funding_grant_id>2024‐A‐001‐CTR</funding_grant_id><funding_grant_id>2024-A-001-CTR</funding_grant_id><funding_grant_id>AARF-22-974065</funding_grant_id><funding_grant_id>AARG-20-683875</funding_grant_id><funding_grant_id>P30AG066506</funding_grant_id><funding_grant_id>P30AG062422</funding_grant_id><funding_grant_id>K23AG073514</funding_grant_id><funding_grant_id>2024-001-1</funding_grant_id><funding_grant_id>2018-A-006-NET</funding_grant_id><funding_grant_id>R01AG045611</funding_grant_id><funding_grant_id>2018‐A‐006‐NET</funding_grant_id><funding_grant_id>K23AG058752</funding_grant_id><funding_grant_id>R01AG048234</funding_grant_id><funding_grant_id>AARF-23-1145318</funding_grant_id><pubmed_authors>Casaletto KB</pubmed_authors><pubmed_authors>Emanuel OM</pubmed_authors><pubmed_authors>DeKosky ST</pubmed_authors><pubmed_authors>Matusz EF</pubmed_authors><pubmed_authors>Loewenstein DA</pubmed_authors><pubmed_authors>Rosselli M</pubmed_authors><pubmed_authors>Barker WW</pubmed_authors><pubmed_authors>Rundek T</pubmed_authors><pubmed_authors>Marsiske M</pubmed_authors><pubmed_authors>Lago AL</pubmed_authors><pubmed_authors>Vaillancourt DE</pubmed_authors><pubmed_authors>Diaz VE</pubmed_authors><pubmed_authors>Asken BM</pubmed_authors><pubmed_authors>DeSimone J</pubmed_authors><pubmed_authors>La Joie R</pubmed_authors><pubmed_authors>Rabinovici GD</pubmed_authors><pubmed_authors>Armstrong MJ</pubmed_authors><pubmed_authors>Arias F</pubmed_authors><pubmed_authors>Rayaprolu S</pubmed_authors><pubmed_authors>Staffaroni A</pubmed_authors><pubmed_authors>VandeVrede L</pubmed_authors><pubmed_authors>Curiel Cid RE</pubmed_authors><pubmed_authors>Webb J</pubmed_authors><pubmed_authors>Wang WE</pubmed_authors><pubmed_authors>Paolillo EW</pubmed_authors><pubmed_authors>Duara R</pubmed_authors><pubmed_authors>Velez-Uribe I</pubmed_authors><pubmed_authors>Kramer JH</pubmed_authors><pubmed_authors>Chan B</pubmed_authors><pubmed_authors>Smith GE</pubmed_authors><pubmed_authors>Lee SY</pubmed_authors><pubmed_authors>Saloner R</pubmed_authors><pubmed_authors>Wiens BA</pubmed_authors><pubmed_authors>Sanderson-Cimino M</pubmed_authors><pubmed_authors>Rojas JC</pubmed_authors><pubmed_authors>Levy SA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Moderating effects of plasma glial fibrillary acidic protein along the Alzheimer's disease continuum.</name><description>&lt;h4>Introduction&lt;/h4>Glial fibrillary acidic protein (GFAP) may contribute to Alzheimer's pathology at early disease stages. GFAP moderation of Alzheimer's disease (AD)-related neurodegeneration and cognition is unclear.&lt;h4>Methods&lt;/h4>We examined plasma GFAP moderation of AD biomarkers (amyloid beta [Aβ]-positron emission tomography [PET][A]; plasma phosphorylated tau-181 [p-tau181][T&lt;sub>1&lt;/sub>]), neurodegeneration (plasma NfL[N&lt;sub>plasma&lt;/sub>]; structural magnetic resonance imaging [MRI][N&lt;sub>MRI&lt;/sub>]), and cognition (Cog&lt;sub>memory&lt;/sub>; Cog&lt;sub>executive&lt;/sub>) in two cohorts: University of California San Francisco (UCSF) (N = 212, 91.0% non-Hispanic/Latino White [NHLW], age = 74.7 [7.6] years, 75.9% cognitively unimpaired [CU]) and 1Florida Alzheimer's Disease Research Centers</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-05-29T22:39:01.75Z</modification><creation>2026-04-08T06:18:57.863Z</creation></dates><accession>S-EPMC12412752</accession><cross_references><pubmed>40911721</pubmed><doi>10.1002/alz.70626</doi></cross_references></HashMap>