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Genetics and molecular pathogenesis of sporadic and hereditary cerebral amyloid angiopathies
Revesz T, Holton JL, Lashley T, Plant G, Frangione B, Rostagno A, Ghiso J.. Acta neuropathologica, 2009-02-19
Topic: Amyloid, tau and blood-test diagnosis
In cerebral amyloid angiopathy (CAA), amyloid fibrils deposit in walls of arteries, arterioles and less frequently in veins and capillaries of the central nervous system, often resulting in secondary degenerative vascular changes. Although the amyloid-beta peptide is by far the commonest amyloid subunit implicated in sporadic and rarely in hereditary forms of CAA, a number of other proteins may also be involved in rare familial diseases in which CAA is also a characteristic morphological feature. These latter proteins include the ABri and ADan subunits in familial British dementia and familial Danish dementia, respectively, which are also known under the umbrella term BRI2 gene-related dementias, variant cystatin C in hereditary cerebral haemorrhage with amyloidosis of Icelandic-type, variant transthyretins in meningo-vascular amyloidosis, disease-associated prion protein (PrP(Sc)) in he
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APA 7th
Revesz, T., Holton, J. L., Lashley, T., Plant, G., Frangione, B., Rostagno, A., et al. (2009). Genetics and molecular pathogenesis of sporadic and hereditary cerebral amyloid angiopathies. Acta neuropathologica. https://doi.org/10.1007/s00401-009-0501-8
Vancouver
Revesz T, Holton JL, Lashley T, Plant G, Frangione B, Rostagno A, et al. Genetics and molecular pathogenesis of sporadic and hereditary cerebral amyloid angiopathies. Acta neuropathologica. 2009. doi:10.1007/s00401-009-0501-8. PMID: 19225789.
BibTeX
@article{revesz2009-19225789,
author = {Revesz, T. and Holton, J. L. and Lashley, T. and Plant, G. and Frangione, B. and Rostagno, A. and Ghiso, J.},
title = {{Genetics and molecular pathogenesis of sporadic and hereditary cerebral amyloid angiopathies}},
journal = {Acta neuropathologica},
year = {2009},
doi = {10.1007/s00401-009-0501-8},
pmid = {19225789},
url = {https://doi.org/10.1007/s00401-009-0501-8}
}
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.
Key findings
- Although the amyloid-beta peptide is by far the commonest amyloid subunit implicated in sporadic and rarely in hereditary forms of CAA, a number of other proteins may also be involved in rare familial diseases in which CAA is also a characteristic morphological feature.
- These latter proteins include the ABri and ADan subunits in familial British dementia and familial Danish dementia, respectively, which are also known under the umbrella term BRI2 gene-related dementias, variant cystatin C in hereditary cerebral haemorrhage with amyloidosis of Icelandic-type, variant transthyretins in meningo-vascular amyloidosis, disease-associated prion protein (PrP(Sc)) in hereditary prion disease with premature stop codon mutations and mutated gelsolin (AGel) in familial amyloidosis of Finnish type.
- In this review, the characteristic morphological features of the different CAAs is described and the implication of the biochemical, genetic and transgenic animal data for the pathogenesis of CAA is discussed.
Why it matters
This paper reviews the genetics and molecular pathogenesis of cerebral amyloid angiopathies, in which amyloid-beta and other proteins deposit in blood vessel walls. It does not report any treatment, cure or prevention for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 49/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Acta neuropathologica) |
| Journal's citation record | 3 / 4 | Acta Neuropathologica: journal h-index 287 (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 | 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 294 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.5 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 4 / 6 | Cited 12.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 9 other studies in this library |
| Still being cited | 2 / 4 | Cited 26 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Jorge A. Ghiso: h-index 79 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19225789) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 49 / 100 | — |
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