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Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers
Clifford R. Jack, David S. Knopman, William J. Jagust, Ronald Carl Petersen, Michael Walter Weiner, Paul S. S. Aisen, Leslie M. Shaw, Prashanthi Vemuri et al.. The Lancet Neurology, 2013-01-16
Topic: Amyloid, tau and blood-test diagnosis
This study updated a 2010 hypothetical model of major Alzheimer's disease (AD) biomarkers based on new evidence. The updated model indexes individuals by time rather than clinical symptom severity and incorporates interindividual variability in cognitive impairment associated with AD pathophysiology progression. It also modifies the temporal ordering of certain biomarkers and hypothesises that in sporadic AD, incident amyloid β pathophysiology can accelerate antecedent limbic and brainstem tauopathy.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Jack, C. R., Knopman, D. S., Jagust, W. J., Petersen, R. C., Weiner, M. W., Aisen, P. S. S., et al. (2013). Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. The Lancet Neurology. https://doi.org/10.1016/s1474-4422(12)70291-0
Vancouver
Jack CR, Knopman DS, Jagust WJ, Petersen RC, Weiner MW, Aisen PSS, et al. Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. The Lancet Neurology. 2013. doi:10.1016/s1474-4422(12)70291-0. PMID: 23332364.
BibTeX
@article{jack2013-23332364,
author = {Jack, Clifford R. and Knopman, David S. and Jagust, William J. and Petersen, Ronald Carl and Weiner, Michael Walter and Aisen, Paul S. S. and Shaw, Leslie M. and Vemuri, Prashanthi and others},
title = {{Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers}},
journal = {The Lancet Neurology},
year = {2013},
doi = {10.1016/s1474-4422(12)70291-0},
pmid = {23332364},
url = {https://doi.org/10.1016/s1474-4422(12)70291-0}
}
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
- Evidence has accumulated that supports the major assumptions of the 2010 hypothetical model of major biomarkers of Alzheimer's disease.
- Refinements to the model include indexing of individuals by time rather than clinical symptom severity.
- The updated model incorporates interindividual variability in cognitive impairment associated with progression of AD pathophysiology.
- The model modifies the specific temporal ordering of some biomarkers.
- The updated model recognizes that amyloid β (Aβ) and tau might be initiated independently in sporadic AD, hypothesising that incident Aβ pathophysiology can accelerate antecedent limbic and brainstem tauopathy.
Why it matters
An updated version of the hypothetical model of how Alzheimer's biomarkers change as the disease progresses. It is still presented as hypothetical, and it is a way of tracking the disease rather than a way of treating or preventing it.
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Study details
- Evidence strengthLow
How this study scored 64/100
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 (The Lancet Neurology) |
| Journal's citation record | 3 / 4 | The Lancet Neurology: journal h-index 457 (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 | 1 / 5 | 2013 — within 20 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 | 7 / 7 | Cited 4,396 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 293.1 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 6 / 6 | Cited 189.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 6 / 6 | Cited by 318 other studies in this library |
| Still being cited | 4 / 4 | Cited 963 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author John Q. Trojanowski: h-index 255 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, Berkeley: institution h-index 2,012 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 23332364) |
| Free to read | 2 / 2 | Free to read |
| Total | 64 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/s1474-4422(12)70291-0
- PubMed: 23332364
- Original source →
- Free full text: PubMed Central →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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