ArticleThe journal of prevention of Alzheimer's disease2025
Utility of plasma GFAP as a secondary endpoint for clinical trials in Alzheimer's disease.
Article in The journal of prevention of Alzheimer's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Blood-based biomarkers and early diagnosis of Alzheimer's disease.Neural regeneration research · 2026Article
- Comparative Prognostic Performance of Hippocampal Volume and Plasma Biomarkers in Amyloid-Negative Subjective Cognitive Decline: A Four-Year Follow-up.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Classification accuracies of plasma ptau217 vs. ptau217/Aβ1-42 for brain Aβ pathology in cognitively normal older adults.GeroScience · 2026Observational
- Cognitive Impairment Associated with Chemotherapy: Neuroimmunological Interactions, Gut-Brain Axis, and Therapeutic Approaches.Brain sciences · 2026Review
- Sex-specific associations between astrocytic reactivity and cognitive decline in unimpaired elderly.bioRxiv : the preprint server for biology · 2026Article
- Hippocampal GFAP in aging: Associations with AD and LATE-NC pathologies and cognitive decline in older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Plasma Biomarkers and Clinical Outcomes in Early-Onset Dementia.JAMA network open · 2026Article
- Clinical impact of the Alzheimer's Disease Neuroimaging Initiative: A review of studies using ADNI data (2023 to June 2025).Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Translating blood-based biomarkers into Alzheimer's disease clinical practice: screening, diagnosis, and longitudinal monitoring.Frontiers in aging neuroscience · 2026Review
- The Role of Glial Fibrillary Acidic Protein in the Neuropathology of Alzheimer's Disease and Its Potential as a Blood Biomarker for Early Diagnosis and Progression.Molecular neurobiology · 2025Review
- Astrocytes provide a unique biomarker for Alzheimer's and other pathologies.The journal of prevention of Alzheimer's disease · 2025Article
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37 authors.
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Abstract
backgroundClinical trials have recently incorporated plasma glial fibrillary acidic protein (GFAP) as an exploratory endpoint. To include plasma GFAP as a secondary endpoint, it is essential to characterize its longitudinal progression in target populations.
objectiveTo evaluate the potential use of plasma GFAP changes as a secondary endpoint in Alzheimer's disease trials.
methodsWe longitudinally evaluated plasma GFAP in individuals with amyloid-beta (Aβ)-PET scans at baseline in three well-characterized cohorts. Cox proportional hazards regression tested the association between changes in plasma GFAP and cognitive function. Analysis of the 95 % confidence interval of annualized change in plasma GFAP provided statistical inference for a significant longitudinal change. Effect size was calculated as the group mean divided by the standard deviation (SD). We estimated the sample size needed to test a 25% drug effect with 80% power on reducing changes in GFAP.
resultsWe assessed 487 individuals [176 cognitively unimpaired (CU; 29% Aβ positive) and 311 cognitively impaired (CI; 51% Aβ positive)] with some degree of cerebrovascular disease (Fazekas 1-3), over a mean (SD) follow-up of 1.84 (0.46) years. Changes in plasma GFAP were significantly associated with worsening in Clinical Dementia Rating sum of boxes (CDR-SB) score across the population (p < 0.0001). In CU, only Aβ positive individuals showed significant changes in GFAP (p < 0.001). On the other hand, both CI Aβ positive and negative individuals showed longitudinal progression in GFAP levels (p < 0.0001). The effect size of changes in plasma GFAP was higher in CU Aβ positive (0.44), followed by CI Aβ positive (0.42) and CI Aβ negative (0.38). Clinical trials focusing on CU Aβ positive would require 1320 individuals per study arm, while focusing on CI Aβ positive would require 1440 individuals per study arm.
conclusionPlasma GFAP increased in parallel with cognitive decline, making it a candidate for monitoring disease progression in trials aimed at mitigating cognitive deterioration. Although Aβ positivity significantly accelerated GFAP progression, the fact that GFAP was increased in CI Aβ negative with cerebrovascular disease supports its potential use as a secondary endpoint in this population as well.
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