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Population variation in glial fibrillary acidic protein levels in brain ageing: relationship to Alzheimer-type pathology and dementia
Wharton SB, O'Callaghan JP, Savva GM, Nicoll JA, Matthews F, Simpson JE, Forster G, Shaw PJ et al.. Dementia and geriatric cognitive disorders, 2009-05-07
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Background The cellular pathology of astrocytes in brain ageing and their role in modulating the brain's response to neurodegenerative pathology remain incompletely understood. Methods Using quantitative ELISA, we have investigated glial fibrillary acidic protein (GFAP) expression in the population-based neuropathology cohort of the Medical Research Council Cognitive Function and Ageing Study to determine: (1) the population variation in the astroglial hypertrophic response, (2) its relationship to the presence of Alzheimer-type pathology, and (3) its association with cognition. Results Increasing GFAP was found with increasing Braak stage, levels increasing even at early stages. Within Braak stages, GFAP did not differ between demented and non-demented individuals, but there was greater variance in GFAP in the demented. Possession of ApoE epsilon4 was associated with slightly increased GFAP levels (not significant) for given amyloid beta protein loads. Conclusion In a population-based sample, increasing gliosis precedes development of Alzheimer lesions. Population variation in GFAP with varying Alzheimer lesion burdens suggests that they are not the only driver for astrogliosis. GFAP was not independently predictive of dementia, but the variation in astrocytic responses may be a factor modulating brain responses to neurodegenerative pathology.
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APA 7th
Wharton, S. B., O'Callaghan, J. P., Savva, G. M., Nicoll, J. A., Matthews, F., Simpson, J. E., et al. (2009). Population variation in glial fibrillary acidic protein levels in brain ageing: relationship to Alzheimer-type pathology and dementia. Dementia and geriatric cognitive disorders. https://doi.org/10.1159/000217729
Vancouver
Wharton SB, O'Callaghan JP, Savva GM, Nicoll JA, Matthews F, Simpson JE, et al. Population variation in glial fibrillary acidic protein levels in brain ageing: relationship to Alzheimer-type pathology and dementia. Dementia and geriatric cognitive disorders. 2009. doi:10.1159/000217729. PMID: 19420941.
BibTeX
@article{wharton2009-19420941,
author = {Wharton, S. B. and O'Callaghan, J. P. and Savva, G. M. and Nicoll, J. A. and Matthews, F. and Simpson, J. E. and Forster, G. and Shaw, P. J. and others},
title = {{Population variation in glial fibrillary acidic protein levels in brain ageing: relationship to Alzheimer-type pathology and dementia}},
journal = {Dementia and geriatric cognitive disorders},
year = {2009},
doi = {10.1159/000217729},
pmid = {19420941},
url = {https://doi.org/10.1159/000217729}
}
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Key findings
- Results Increasing GFAP was found with increasing Braak stage, levels increasing even at early stages.
- Possession of ApoE epsilon4 was associated with slightly increased GFAP levels (not significant) for given amyloid beta protein loads.
- Population variation in GFAP with varying Alzheimer lesion burdens suggests that they are not the only driver for astrogliosis.
Why it matters
In a population-based sample, GFAP increased with increasing Braak stage, even at early stages, but within Braak stages GFAP did not differ between demented and non-demented individuals, and it was not independently predictive of dementia. This suggests that astrogliosis is not solely driven by Alzheimer lesions and does not by itself predict dementia.
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Study details
- Evidence strengthModerate
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Dementia and geriatric cognitive disorders) |
| Journal's citation record | 1 / 4 | Dementia and Geriatric Cognitive Disorders: journal h-index 149 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2009 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 58 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.1 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 3 / 6 | Cited 4.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 1 / 4 | Cited 4 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Paul G. Ince: h-index 102 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Cambridge: institution h-index 1,973 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19420941) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 44 / 100 | — |
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