CSF fibrinogen predicts longitudinal Tau accumulation in cognitively unimpaired older adults.

Publication Type Academic Article
Authors Lisgaras C, Jacobs T, Figueredo L, Pirraglia E, Radtke C, Keller J, Karvelas N, Bernal J, Ruiz J, Zetterberg H, Glodzik L, de Leon M, McIntire L, Boutajangout A, Wisniewski T, Ramos-Cejudo J, Alcolea D, Giménez S, Fortea J, Akassoglou K, Elahi F, Osorio R
Journal Alzheimers Dement
Volume 22
Issue 8
Pagination e71720
Date Published 08/01/2026
ISSN 1552-5279
Keywords tau Proteins, Fibrinogen
Abstract INTRODUCTION: Blood-brain barrier (BBB) dysfunction is an early feature of Alzheimer's disease (AD). Fibrinogen represents a sensitive marker of BBB leakage, but whether it modifies longitudinal tau progression in cognitively unimpaired (CU) individuals remains unknown. METHODS: CU older adults underwent clinical evaluation and cerebrospinal fluid (CSF) assessment of fibrinogen, Aβ42, total tau (tTau), phosphorylated tau 181 (pTau181), and YKL-40. Linear regression tested baseline associations. Linear mixed-effects models tested whether baseline fibrinogen predicted longitudinal pTau181 change. RESULTS: Among 169 CU participants with baseline fibrinogen, 87 had longitudinal pTau181 measurements (mean follow-up 2.5-years). Higher fibrinogen was associated with elevated YKL-40 (β = 0.28, 95% confidence interval [CI] [0.11, 0.45]) but not Aβ42, tTau, or pTau181 at baseline. Baseline fibrinogen modified longitudinal pTau181 trajectories (interaction β = 0.11, 95% CI [0.04, 0.19]), with only participants above the median showing significant pTau181 increases (β = 0.13, 95% CI [0.08, 0.18]). DISCUSSION: CSF fibrinogen associates cross-sectionally with glial inflammation and predicts accelerated tau accumulation in preclinical AD.
DOI 10.1002/alz.71720
PubMed ID 42583778
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