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Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline
Rabin JS, Nichols E, La Joie R, Casaletto KB, Palta P, Dams-O'Connor K, Kumar RG, George KM et al.. Brain : a journal of neurology, 2022-08-01
Topic: Amyloid, tau and blood-test diagnosis
Accumulating data suggest that cerebrovascular disease contributes to Alzheimer's disease pathophysiology and progression toward dementia. Cerebral amyloid angiopathy is a form of cerebrovascular pathology that results from the build-up of β-amyloid in the vessel walls. We used linear regression and linear mixed models to test independent versus interactive associations of cerebral amyloid angiopathy and neuritic plaque burden with tau burden and longitudinal cognitive decline, respectively. These results highlight the dynamic interplay between cerebral amyloid angiopathy and Alzheimer's disease pathology in accelerating progression toward dementia. These findings have implications for Alzheimer's disease clinical trials and therapeutic development.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Rabin, J. S., Nichols, E., La Joie, R., Casaletto, K. B., Palta, P., Dams-O'Connor, K., et al. (2022). Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline. Brain : a journal of neurology. https://doi.org/10.1093/brain/awac178
Vancouver
Rabin JS, Nichols E, La Joie R, Casaletto KB, Palta P, Dams-O'Connor K, et al. Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline. Brain : a journal of neurology. 2022. doi:10.1093/brain/awac178. PMID: 35759327.
BibTeX
@article{rabin2022-35759327,
author = {Rabin, J. S. and Nichols, E. and La Joie, R. and Casaletto, K. B. and Palta, P. and Dams-O'Connor, K. and Kumar, R. G. and George, K. M. and others},
title = {{Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline}},
journal = {Brain : a journal of neurology},
year = {2022},
doi = {10.1093/brain/awac178},
pmid = {35759327},
url = {https://doi.org/10.1093/brain/awac178}
}
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Key findings
- Accumulating data suggest that cerebrovascular disease contributes to Alzheimer's disease pathophysiology and progression toward dementia.
- Cerebral amyloid angiopathy is a form of cerebrovascular pathology that results from the build-up of β-amyloid in the vessel walls.
- We used linear regression and linear mixed models to test independent versus interactive associations of cerebral amyloid angiopathy and neuritic plaque burden with tau burden and longitudinal cognitive decline, respectively.
- These results highlight the dynamic interplay between cerebral amyloid angiopathy and Alzheimer's disease pathology in accelerating progression toward dementia.
- These findings have implications for Alzheimer's disease clinical trials and therapeutic development.
Why it matters
This cohort study found that cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline. The findings suggest implications for Alzheimer's disease clinical trials and therapeutic development, but no treatment, cure or prevention was tested.
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Study details
- Study designcohort study
- Participants1,722
- Evidence strengthModerate
How this study scored 67/100
Published in a leading specialty journal, and it is a cohort study following people over time. Scored zero for effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Brain : a journal of neurology) |
| Journal's citation record | 4 / 4 | Brain: journal h-index 503 (OpenAlex, 2026-10-29) |
| Study design | 7 / 12 | A cohort study following people over time |
| 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 | 3 / 5 | 2022 — within 6 year(s) of the newest study here |
| Sample size | 3 / 4 | 1,722 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 77 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.8 citations a year over 6 year(s) since 2022 |
| Impact for its field and year | 3 / 6 | Cited 8.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 3 / 4 | Cited 65 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Adam M. Brickman: h-index 87 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Johns Hopkins University: institution h-index 2,306 (OpenAlex) |
| Multicenter collaboration | 3 / 3 | OpenAlex lists 14 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 35759327) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 67 / 100 | — |
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