Abstract | INTRODUCTION: METHOD: One hundred sixty MCI patients were followed for 4.7 years (average). AD pathology was defined using cerebrospinal fluid (CSF) Aβ42/40 and Aβ42/total tau (T-tau). Plasma GFAP was measured at baseline and follow-up using Simoa technology. RESULTS: Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72-0.86) and 0.80 (95% CI 0.72-0.86), respectively. When also including APOE ε4 status as a predictor, the accuracy of the model to detect abnormal CSF Aβ42/40 status improved (AUC = 0.86, p = 0.02). Plasma GFAP predicted subsequent conversion to AD dementia with an AUC of 0.84 (95% CI 0.77-0.91), which was not significantly improved when adding APOE ε4 or age as predictors to the model. Longitudinal GFAP slopes for Aβ-positive and MCI who progressed to dementia (AD or other) were significantly steeper than those for Aβ-negative (p = 0.007) and stable MCI (p < 0.0001), respectively. CONCLUSION: Plasma GFAP can detect AD pathology in patients with MCI and predict conversion to AD dementia.
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Authors | Claudia Cicognola, Shorena Janelidze, Joakim Hertze, Henrik Zetterberg, Kaj Blennow, Niklas Mattsson-Carlgren, Oskar Hansson |
Journal | Alzheimer's research & therapy
(Alzheimers Res Ther)
Vol. 13
Issue 1
Pg. 68
(03 27 2021)
ISSN: 1758-9193 [Electronic] England |
PMID | 33773595
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Amyloid beta-Peptides
- Biomarkers
- GFAP protein, human
- Glial Fibrillary Acidic Protein
- Peptide Fragments
- tau Proteins
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Topics |
- Alzheimer Disease
(complications, diagnosis, genetics)
- Amyloid beta-Peptides
- Biomarkers
- Cognitive Dysfunction
(diagnosis)
- Glial Fibrillary Acidic Protein
(blood, metabolism)
- Humans
- Peptide Fragments
- tau Proteins
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