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Association of Apolipoprotein E ε4 With Medial Temporal Tau Independent of Amyloid-β
Therriault J, Benedet AL, Pascoal TA, Mathotaarachchi S, Chamoun M, Savard M, Thomas E, Kang MS et al.. JAMA neurology, 2020-04-01
Topic: Brain proteins, microglia and lab models
While APOEε4 is associated with increased amyloid-β burden, its association with cerebral tau pathology has been controversial. Objective To determine whether APOEε4 is associated with medial temporal tau pathology independently of amyloid-β, sex, clinical status, and age. Results The mean (SD) age of the 489 participants was 70.5 (7.1) years; 171 were APOEε4 carriers (34.9%), and 230 of 489 were men. In both cohorts, APOEε4 was associated in increased tau-PET uptake in the entorhinal cortex and hippocampus independently of amyloid-β, sex, age, and clinical status after multiple comparisons correction (TRIAD: β = 0.33; 95% CI, 0.19-0.49; ADNI: β = 0.13; 95% CI, 0.08-0.19; P Conclusions and relevance Our results indicate that the elevated risk of developing dementia conferred by APOEε4 genotype involves mechanisms associated with both amyloid-β and tau aggregation. These results contribute to an evolving framework in which APOEε4 has deleterious consequences in Alzheimer disease beyond its link with amyloid-β and suggest APOEε4 as a potential target for future disease-modifying therapeutic trials targeting tau pathology.
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APA 7th
Therriault, J., Benedet, A. L., Pascoal, T. A., Mathotaarachchi, S., Chamoun, M., Savard, M., et al. (2020). Association of Apolipoprotein E ε4 With Medial Temporal Tau Independent of Amyloid-β. JAMA neurology. https://doi.org/10.1001/jamaneurol.2019.4421
Vancouver
Therriault J, Benedet AL, Pascoal TA, Mathotaarachchi S, Chamoun M, Savard M, et al. Association of Apolipoprotein E ε4 With Medial Temporal Tau Independent of Amyloid-β. JAMA neurology. 2020. doi:10.1001/jamaneurol.2019.4421. PMID: 31860000.
BibTeX
@article{therriault2020-31860000,
author = {Therriault, J. and Benedet, A. L. and Pascoal, T. A. and Mathotaarachchi, S. and Chamoun, M. and Savard, M. and Thomas, E. and Kang, M. S. and others},
title = {{Association of Apolipoprotein E ε4 With Medial Temporal Tau Independent of Amyloid-β}},
journal = {JAMA neurology},
year = {2020},
doi = {10.1001/jamaneurol.2019.4421},
pmid = {31860000},
url = {https://doi.org/10.1001/jamaneurol.2019.4421}
}
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.
Key findings
- While APOEε4 is associated with increased amyloid-β burden, its association with cerebral tau pathology has been controversial.
- Objective To determine whether APOEε4 is associated with medial temporal tau pathology independently of amyloid-β, sex, clinical status, and age.
- Results The mean (SD) age of the 489 participants was 70.5 (7.1) years; 171 were APOEε4 carriers (34.9%), and 230 of 489 were men.
- In both cohorts, APOEε4 was associated in increased tau-PET uptake in the entorhinal cortex and hippocampus independently of amyloid-β, sex, age, and clinical status after multiple comparisons correction (TRIAD: β = 0.33; 95% CI, 0.19-0.49; ADNI: β = 0.13; 95% CI, 0.08-0.19; P < .001).
- These results contribute to an evolving framework in which APOEε4 has deleterious consequences in Alzheimer disease beyond its link with amyloid-β and suggest APOEε4 as a potential target for future disease-modifying therapeutic trials targeting tau pathology.
Why it matters
APOE ε4 was associated with increased tau PET uptake in the entorhinal cortex and hippocampus independently of amyloid-β, sex, age and clinical status. The authors suggest APOE ε4 as a potential target for future disease-modifying trials targeting tau pathology, but no treatment was tested.
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Study details
- Study designcross-sectional
- Participants124
- Effect size34.9%
- Evidence strengthModerate
How this study scored 64/100
Published in a leading specialty journal, and it is a snapshot of people at one point in time. Scored zero for randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (JAMA neurology) |
| Journal's citation record | 2 / 4 | JAMA Neurology: journal h-index 235 (OpenAlex, 2026-10-29) |
| Study design | 4 / 12 | A snapshot of people at one point in 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 | 2 / 5 | 2020 — within 10 year(s) of the newest study here |
| Sample size | 2 / 4 | 124 participants |
| Effect reported | 2 / 3 | Effect reported as a number, without an interval or test |
| 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 | 5 / 7 | Cited 261 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 32.6 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 4 / 6 | Cited 15.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 27 other studies in this library |
| Still being cited | 3 / 4 | Cited 99 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Pedro Rosa‐Neto: h-index 89 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | McGill University: institution h-index 1,373 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31860000) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 64 / 100 | — |
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Read the original
- DOI: 10.1001/jamaneurol.2019.4421
- PubMed: 31860000
- 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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