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Cerebral amyloid angiopathies: a pathologic, biochemical, and genetic view
Revesz T, Ghiso J, Lashley T, Plant G, Rostagno A, Frangione B, Holton JL.. Journal of neuropathology and experimental neurology, 2003-09-01
Topic: Amyloid, tau and blood-test diagnosis
Amyloid deposition can take place in the walls of arteries, arterioles, and, less often, capillaries and veins of the central nervous system, a phenomenon known as cerebral amyloid angiopathy (CAA). The major clinicopathological manifestations of CAA include cerebral hemorrhage, ischemic lesions, and dementia. CAA may be classified according to the amyloid protein deposited.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Revesz, T., Ghiso, J., Lashley, T., Plant, G., Rostagno, A., Frangione, B., et al. (2003). Cerebral amyloid angiopathies: a pathologic, biochemical, and genetic view. Journal of neuropathology and experimental neurology. https://doi.org/10.1093/jnen/62.9.885
Vancouver
Revesz T, Ghiso J, Lashley T, Plant G, Rostagno A, Frangione B, et al. Cerebral amyloid angiopathies: a pathologic, biochemical, and genetic view. Journal of neuropathology and experimental neurology. 2003. doi:10.1093/jnen/62.9.885. PMID: 14533778.
BibTeX
@article{revesz2003-14533778,
author = {Revesz, T. and Ghiso, J. and Lashley, T. and Plant, G. and Rostagno, A. and Frangione, B. and Holton, J. L.},
title = {{Cerebral amyloid angiopathies: a pathologic, biochemical, and genetic view}},
journal = {Journal of neuropathology and experimental neurology},
year = {2003},
doi = {10.1093/jnen/62.9.885},
pmid = {14533778},
url = {https://doi.org/10.1093/jnen/62.9.885}
}
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
- The major clinicopathological manifestations of CAA include cerebral hemorrhage, ischemic lesions, and dementia.
- CAA may be classified according to the amyloid protein deposited.
- In the most common form, sporadic CAA, and in CAA related to sporadic Alzheimer disease (AD).
- CAA can also be severe in variants of familial AD caused by mutations of the amyloid-beta precursor protein or presenilin-1 genes in which deposition of A beta variants and/or wild-type A beta occurs.
Why it matters
This review describes cerebral amyloid angiopathy, in which amyloid deposits in blood vessel walls can cause cerebral hemorrhage, ischemic lesions and dementia, and notes that it can be severe in some familial forms of Alzheimer's disease. It explains disease mechanisms and does not test any treatment or prevention.
Study details
- Evidence strengthLow
How this study scored 47/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 2003 — 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 | 5 / 7 | Cited 287 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.5 citations a year over 25 year(s) since 2003 |
| Impact for its field and year | 4 / 6 | Cited 11.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 13 other studies in this library |
| Still being cited | 2 / 4 | Cited 15 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Janice L. Holton: h-index 89 (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 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 14533778) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 47 / 100 | — |
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