Plasma glial fibrillary acidic protein is elevated in cognitively normal older adults at risk of Alzheimer’s disease
Open accessAbstract
Glial fibrillary acidic protein (GFAP), an astrocytic cytoskeletal protein, can be measured in blood samples, and has been associated with Alzheimer’s disease (AD). However, plasma GFAP has not been investigated in cognitively normal older adults at risk of AD, based on brain amyloid-β (Aβ) load. Cross-sectional analyses were carried out for plasma GFAP and plasma Aβ1–42/Aβ1–40 ratio, a blood-based marker associated with brain Aβ load, in participants (65–90 years) categorised into low (Aβ−, n = 63) and high (Aβ+, n = 33) brain Aβ load groups via Aβ positron emission tomography. Plasma GFAP, Aβ1–42, and Aβ1–40 were measured using the Single molecule array (Simoa) platform. Plasma GFAP levels were significantly higher ( p < 0.00001), and plasma Aβ1–42/Aβ1–40 ratios were significantly lower ( p < 0.005), in Aβ+ participants compared to Aβ− participants, adjusted for covariates age, sex, and apolipoprotein E-ε4 carriage. A receiver operating characteristic curve based on a logistic regression of the same covariates, the base model, distinguished Aβ+ from Aβ− (area under the curve, AUC = 0.78), but was outperformed when plasma GFAP was added to the base model (AUC = 0.91) and further improved with plasma Aβ1–42/Aβ1–40 ratio (AUC = 0.92). The current findings demonstrate that plasma GFAP levels are elevated in cognitively normal older adults at risk of AD. These observations suggest that astrocytic damage or activation begins from the pre-symptomatic stage of AD and is associated with brain Aβ load. Observations from the present study highlight the potential of plasma GFAP to contribute to a diagnostic blood biomarker panel (along with plasma Aβ1–42/Aβ1–40 ratios) for cognitively normal older adults at risk of AD.
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The more pronounced group differences in blood could suggest an association of GFAP levels with amyloidosis.
“The more pronounced group differences in blood could suggest an association of GFAP levels with amyloidosis [76–79].”
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- Authors
- Chatterjee, P., Pedrini, S., Stoops, E., Goozee, K., Villemagne, V. L., Asih, P. R., Verberk, I. M. W., Dave, P., Taddei, K., Sohrabi, H. R., Zetterberg, H., Blennow, K., Teunissen, C. E., Vanderstichele, H. M., & Martins, R. N.
- Affiliations
- Edith Cowan University (AU)
- ADx NeuroSciences (BE)
- Austin Hospital (AU)
- Macquarie University (AU)
- Amsterdam Neuroscience (NL)
- Sahlgrenska University Hospital (SE)
- Corresponding author
- Martins, Ralph N.
- ORCID
- Venue
- Translational Psychiatry
- Published
- 2021-01-11
- Volume
- 11
- Issue
- 1
- Pages
- 27-27
- ISSN
- 2158-3188 (ISSN-L)
- PMC
- PMC7801513
- OpenAlex
- W3108081750
- Cited by
- 439
- References
- 52
- Citations by year
- 2026: 54 · 2025: 80 · 2024: 114 · 2023: 98 · 2022: 60 · 2021: 31 · 2020: 1 · 2015: 1
- FWCI
- 54.30
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Translational Psychiatry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion, other-oa)
- Australasian Journal of Paramedicine (submittedVersion, cc-by)
- Murdoch University Research Portal (submittedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- Svenska Forskningsrådet Formas (2018-02532, 2017-00915)
- Alzheimer’s Drug Discovery Foundation (RDAPB-201809-2016615)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- glial fibrillary acidic protein, plasma biomarkers, Alzheimer's disease, amyloid-beta, preclinical Alzheimer's disease, cognitively normal older adults, astrocyte activation, blood-based biomarkers, amyloid PET, APOE ε4, diagnostic biomarker panel
- MeSH terms
- Aged, Alzheimer Disease, Cross-Sectional Studies, Glial Fibrillary Acidic Protein, Humans, Peptide Fragments, Amyloid beta-Peptides, Apolipoprotein E4
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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