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Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease
Bejanin A, Schonhaut DR, La Joie R, Kramer JH, Baker SL, Sosa N, Ayakta N, Cantwell A et al.. Brain : a journal of neurology, 2017-12-01
Topic: Amyloid, tau and blood-test diagnosis
Neuropathological and in vivo studies have revealed a tight relationship between tau pathology and cognitive impairment across the Alzheimer's disease spectrum. However, tau pathology is also intimately associated with neurodegeneration and amyloid pathology. Our results showed that decreased cognitive performance in each domain was related to increased 18F-AV-1451 binding in specific brain regions conforming to established brain-behaviour relationships (i.e. episodic memory: medial temporal lobe and angular gyrus; semantic memory: left anterior temporal regions; language: left posterior superior temporal lobe and supramarginal gyrus; executive functions: bilateral frontoparietal regions; visuospatial functions: right more than left occipitotemporal regions). Mediation analyses revealed both direct and grey matter-mediated effects of 18F-AV-1451 uptake on cognitive performance. Together, these results show that tau pathology is related in a region-specific manner to cognitive impairment in Alzheimer's disease. This suggests that tau pathology may lead to cognitive deficits through a variety of mechanisms, including, but not restricted to, grey matter loss. These results might have implications for future therapeutic trials targeting tau pathology.
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APA 7th
Bejanin, A., Schonhaut, D. R., La Joie, R., Kramer, J. H., Baker, S. L., Sosa, N., et al. (2017). Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease. Brain : a journal of neurology. https://doi.org/10.1093/brain/awx243
Vancouver
Bejanin A, Schonhaut DR, La Joie R, Kramer JH, Baker SL, Sosa N, et al. Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease. Brain : a journal of neurology. 2017. doi:10.1093/brain/awx243. PMID: 29053874.
BibTeX
@article{bejanin2017-29053874,
author = {Bejanin, A. and Schonhaut, D. R. and La Joie, R. and Kramer, J. H. and Baker, S. L. and Sosa, N. and Ayakta, N. and Cantwell, A. and others},
title = {{Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease}},
journal = {Brain : a journal of neurology},
year = {2017},
doi = {10.1093/brain/awx243},
pmid = {29053874},
url = {https://doi.org/10.1093/brain/awx243}
}
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Key findings
- Neuropathological and in vivo studies have revealed a tight relationship between tau pathology and cognitive impairment across the Alzheimer's disease spectrum.
- However, tau pathology is also intimately associated with neurodegeneration and amyloid pathology.
- Our results showed that decreased cognitive performance in each domain was related to increased 18F-AV-1451 binding in specific brain regions conforming to established brain-behaviour relationships (i.e. episodic memory: medial temporal lobe and angular gyrus; semantic memory: left anterior temporal regions; language: left posterior superior temporal lobe and supramarginal gyrus; executive functions: bilateral frontoparietal regions; visuospatial functions: right more than left occipitotemporal regions).
- Mediation analyses revealed both direct and grey matter-mediated effects of 18F-AV-1451 uptake on cognitive performance.
- Together, these results show that tau pathology is related in a region-specific manner to cognitive impairment in Alzheimer's disease.
Why it matters
This study found that tau pathology was related in a region-specific way to cognitive impairment in Alzheimer's disease, partly through grey matter loss. The authors suggest these results might have implications for future therapeutic trials targeting tau pathology, but no treatment was tested here.
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Study details
- Participants40
- Evidence strengthLow
How this study scored 63/100
Published in a leading specialty journal. Scored zero for study design, effect reported and randomised / 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 | 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 | 2 / 5 | 2017 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 40 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 | 6 / 7 | Cited 787 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 71.5 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 5 / 6 | Cited 38.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 48 other studies in this library |
| Still being cited | 4 / 4 | Cited 301 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Gil D. Rabinovici: h-index 116 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, Berkeley: institution h-index 2,012 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29053874) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 63 / 100 | — |
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