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Cerebral Amyloid Angiopathy Pathology and Its Association With Amyloid-β PET Signal
McCarter SJ, Lesnick TG, Lowe V, Mielke MM, Constantopoulos E, Rabinstein AA, Przybelski SA, Botha H et al.. Neurology, 2021-09-09
Topic: Amyloid, tau and blood-test diagnosis
Background and objectives To determine the contribution of cerebral amyloid angiopathy (CAA) to Pittsburgh compound B (PiB)-PET tracer retention. Methods Participants from the Mayo Clinic Study of Aging and Mayo Clinic Alzheimer's Disease Research Center with antemortem PiB-PET imaging for β-amyloid (Aβ) who later underwent autopsy were included in this study. Pathologic regional leptomeningeal, parenchymal, capillary CAA, and Aβ plaque burden were calculated from one hemisphere. Regional lobar amyloid standardized uptake value ratio (SUVR) on PET was calculated from the same hemisphere sampled at autopsy. Single- and multiple-predictor linear regression models were used to evaluate the relative contributions of pathologically determined regional CAA and Aβ plaques to antemortem PiB-PET SUVR. Results Forty-one participants (30 male, 11 female) with a mean (SD) age at death of 75.7 (10.6) years were included. Twenty-seven (66%) had high PiB signal with a mean (SD) of 2.3 (1.2) years from time of PET scan to death; 24 (59%) had a pathologic diagnosis of Alzheimer disease. On multivariate analysis, CAA was not associated with PiB-PET SUVR, while plaques remained associated with PiB-PET SUVR in all regions (all p Discussion We did not find evidence that pathologically confirmed regional CAA burden contributes significantly to proximal antemortem regional PiB-PET signal, suggesting that amyloid PET imaging for measurement of cortical amyloid burden is unconfounded by CAA on a lobar level. Whether CAA burden contributes to PiB-PET signal in patients with severe CAA phenotypes, such as lobar hemorrhage, requires further investigation.
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APA 7th
McCarter, S. J., Lesnick, T. G., Lowe, V., Mielke, M. M., Constantopoulos, E., Rabinstein, A. A., et al. (2021). Cerebral Amyloid Angiopathy Pathology and Its Association With Amyloid-β PET Signal. Neurology. https://doi.org/10.1212/wnl.0000000000012770
Vancouver
McCarter SJ, Lesnick TG, Lowe V, Mielke MM, Constantopoulos E, Rabinstein AA, et al. Cerebral Amyloid Angiopathy Pathology and Its Association With Amyloid-β PET Signal. Neurology. 2021. doi:10.1212/wnl.0000000000012770. PMID: 34504022.
BibTeX
@article{mccarter2021-34504022,
author = {McCarter, S. J. and Lesnick, T. G. and Lowe, V. and Mielke, M. M. and Constantopoulos, E. and Rabinstein, A. A. and Przybelski, S. A. and Botha, H. and others},
title = {{Cerebral Amyloid Angiopathy Pathology and Its Association With Amyloid-β PET Signal}},
journal = {Neurology},
year = {2021},
doi = {10.1212/wnl.0000000000012770},
pmid = {34504022},
url = {https://doi.org/10.1212/wnl.0000000000012770}
}
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Key findings
- Results Forty-one participants (30 male, 11 female) with a mean (SD) age at death of 75.7 (10.6) years were included.
- On multivariate analysis, CAA was not associated with PiB-PET SUVR, while plaques remained associated with PiB-PET SUVR in all regions (all p < 0.05).
Why it matters
In 41 autopsied participants, cerebral amyloid angiopathy burden was not associated with PiB-PET signal, while amyloid plaques were associated in all regions. This is a pathology-imaging correlation study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 45/100
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 (Neurology) |
| Journal's citation record | 4 / 4 | Neurology: journal h-index 525 (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 | 3 / 5 | 2021 — within 6 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 | 3 / 7 | Cited 26 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.7 citations a year over 7 year(s) since 2021 |
| Impact for its field and year | 2 / 6 | Cited 1.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 2 / 4 | Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Jonathan Graff‐Radford: h-index 73 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Mayo Clinic: institution h-index 1,606 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 34504022) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
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Read the original
- DOI: 10.1212/wnl.0000000000012770
- PubMed: 34504022
- Original source →
- Free full text: PubMed Central →
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
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