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Neuroinflammation in Alzheimer's disease and prion disease
Eikelenboom P, Bate C, Van Gool WA, Hoozemans JJM, Rozemuller JM, Veerhuis R, Williams A.. Glia, 2002-11-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) and prion disease are characterized neuropathologically by extracellular deposits of Abeta and PrP amyloid fibrils, respectively. In both disorders, these cerebral amyloid deposits are co-localized with a broad variety of inflammation-related proteins (complement factors, acute-phase protein, pro-inflammatory cytokines) and clusters of activated microglia. The present data suggest that the cerebral Abeta and PrP deposits are closely associated with a locally induced, non-immune-mediated chronic inflammatory response.
Key findings
- In both disorders, these cerebral amyloid deposits are co-localized with a broad variety of inflammation-related proteins (complement factors, acute-phase protein, pro-inflammatory cytokines) and clusters of activated microglia.
- The present data suggest that the cerebral Abeta and PrP deposits are closely associated with a locally induced, non-immune-mediated chronic inflammatory response.
- Epidemiological studies indicate that polymorphisms of certain cytokines and acute-phase proteins, which are associated with Abeta plaques, are genetic risk factors for AD.
- Transgenic mice studies have established the role of amyloid associated acute-phase proteins in Alzheimer amyloid formation.
Why it matters
This work reports that amyloid deposits in Alzheimer's disease and prion disease are accompanied by inflammation-related proteins and activated microglia, suggesting a locally induced chronic inflammatory response. It describes an association in tissue and does not show that reducing this inflammation treats or prevents the disease.
Study details
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 44 of the 96 points we could judge it on, which is 46 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Glia) |
| Journal's citation record | 2 / 4 | Glia: journal h-index 233 (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 | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2002 — older than 20 years, still counted |
| 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 407 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.7 citations a year over 26 year(s) since 2002 |
| Impact for its field and year | 4 / 6 | Cited 12.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 10 other studies in this library |
| Still being cited | 1 / 4 | Cited 7 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | 2 / 3 | University of Glasgow: institution h-index 1,600 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 12379910) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 44 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 44 of the 96 points we could judge it on is 46 out of 100. |
| Total | 46 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
APA 7th
Eikelenboom, P., Bate, C., Van Gool, W. A., Hoozemans, J. J. M., Rozemuller, J. M., Veerhuis, R., et al. (2002). Neuroinflammation in Alzheimer's disease and prion disease. Glia. https://doi.org/10.1002/glia.10146
Vancouver
Eikelenboom P, Bate C, Van Gool WA, Hoozemans JJM, Rozemuller JM, Veerhuis R, et al. Neuroinflammation in Alzheimer's disease and prion disease. Glia. 2002. doi:10.1002/glia.10146. PMID: 12379910.
BibTeX
@article{eikelenboom2002-12379910,
author = {Eikelenboom, P. and Bate, C. and Van Gool, W. A. and Hoozemans, J. J. M. and Rozemuller, J. M. and Veerhuis, R. and Williams, A.},
title = {{Neuroinflammation in Alzheimer's disease and prion disease}},
journal = {Glia},
year = {2002},
doi = {10.1002/glia.10146},
pmid = {12379910},
url = {https://doi.org/10.1002/glia.10146}
}
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