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Tau and Amyloid Relationships with Resting-state Functional Connectivity in Atypical Alzheimer's Disease
Irene Sintini, Jonathan Graff-Radford, David T Jones, Hugo Botha, Peter R Martin, Mary M Machulda, Christopher G Schwarz, Matthew L Senjem et al.. Cerebral cortex (New York, N.Y. : 1991), 2021-02-05
Topic: Plasma and spinal-fluid biomarkers
The mechanisms through which tau and amyloid-beta (Aβ) accumulate in the brain of Alzheimer's disease patients may differ but both are related to neuronal networks. We examined such mechanisms on neuroimaging in 58 participants with atypical Alzheimer's disease (posterior cortical atrophy or logopenic progressive aphasia). Participants underwent Aβ-PET, longitudinal tau-PET, structural MRI and resting-state functional MRI, which was analyzed with graph theory. Regions with high levels of Aβ were more likely to be functional hubs, with a high number of functional connections important for resilience to cascading network failures. Regions with high levels of tau were more likely to have low clustering coefficients and degrees, suggesting a lack of trophic support or vulnerability to local network failures. Regions strongly functionally connected to the disease epicenters were more likely to have higher levels of tau and, less strongly, of Aβ. The regional rate of tau accumulation was associated with tau levels in functionally connected regions, in support of tau accumulation in a functional network. This study elucidates the relations of tau and Aβ to functional connectivity metrics in atypical Alzheimer's disease, strengthening the hypothesis that the spread of the 2 proteins is driven by different biological mechanisms related to functional networks.
Key findings
- The regional rate of tau accumulation was associated with tau levels in functionally connected regions, in support of tau accumulation in a functional network.
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Study details
- Study designlongitudinal study
- Participants58
- Evidence strengthModerate
How this study scored 64/100
Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 36 of the 56 points we could judge it on, which is 64 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Cerebral cortex (New York, N.Y. : 1991)) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 7 / 12 | A longitudinal study following the same 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 | 2021 — within 6 year(s) of the newest study here |
| Sample size | 1 / 4 | 58 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 33152765) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 36 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 36 of the 56 points we could judge it on is 64 out of 100. |
| Total | 64 / 100 | — |
What each of these 20 components measures, and what this score is not →
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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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Sintini, I., Graff-Radford, J., Jones, D. T., Botha, H., Martin, P. R., Machulda, M. M., et al. (2021). Tau and Amyloid Relationships with Resting-state Functional Connectivity in Atypical Alzheimer's Disease. Cerebral cortex (New York, N.Y. : 1991). https://doi.org/10.1093/cercor/bhaa319
Vancouver
Sintini I, Graff-Radford J, Jones DT, Botha H, Martin PR, Machulda MM, et al. Tau and Amyloid Relationships with Resting-state Functional Connectivity in Atypical Alzheimer's Disease. Cerebral cortex (New York, N.Y. : 1991). 2021. doi:10.1093/cercor/bhaa319. PMID: 33152765.
BibTeX
@article{sintini2021-33152765,
author = {Sintini, Irene and Graff-Radford, Jonathan and Jones, David T and Botha, Hugo and Martin, Peter R and Machulda, Mary M and Schwarz, Christopher G and Senjem, Matthew L and others},
title = {{Tau and Amyloid Relationships with Resting-state Functional Connectivity in Atypical Alzheimer's Disease}},
journal = {Cerebral cortex (New York, N.Y. : 1991)},
year = {2021},
doi = {10.1093/cercor/bhaa319},
pmid = {33152765},
url = {https://doi.org/10.1093/cercor/bhaa319}
}
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