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