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Proteomics of brain, CSF, and plasma identifies molecular signatures for distinguishing sporadic and genetic Alzheimer's disease
Sung YJ, Yang C, Norton J, Johnson M, Fagan A, Bateman RJ, Perrin RJ, Morris JC et al.. Science translational medicine, 2023-07-05
Topic: Amyloid, tau and blood-test diagnosis
Proteomic studies for Alzheimer's disease (AD) are instrumental in identifying AD pathways but often focus on single tissues and sporadic AD cases. Here, we present a proteomic study analyzing 1305 proteins in brain tissue, cerebrospinal fluid (CSF), and plasma from patients with sporadic AD, TREM2 risk variant carriers, patients with autosomal dominant AD (ADAD), and healthy individuals. We identified 8 brain, 40 CSF, and 9 plasma proteins that were altered in individuals with sporadic AD, and we replicated these findings in several external datasets.
Key findings
- Here, we present a proteomic study analyzing 1305 proteins in brain tissue, cerebrospinal fluid (CSF), and plasma from patients with sporadic AD, TREM2 risk variant carriers, patients with autosomal dominant AD (ADAD), and healthy individuals.
- We identified 8 brain, 40 CSF, and 9 plasma proteins that were altered in individuals with sporadic AD, and we replicated these findings in several external datasets.
- We identified a proteomic signature that differentiated TREM2 variant carriers from both individuals with sporadic AD and healthy individuals.
- The proteins associated with sporadic AD were also altered in patients with ADAD, but with a greater effect size.
Why it matters
This proteomic study measured proteins in brain, cerebrospinal fluid, and plasma and found signatures that distinguished sporadic Alzheimer's disease and TREM2 variant carriers from controls. It is about molecular signatures and diagnosis, not about treating, curing, or preventing the disease.
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Study details
- Evidence strengthLow
How this study scored 52/100
Published in a peer-reviewed 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 | 7 / 10 | Tier 3 — peer-reviewed journal (Science translational medicine) |
| Journal's citation record | 3 / 4 | Science Translational Medicine: journal h-index 365 (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 | 2023 — 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 | 4 / 7 | Cited 85 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 17.0 citations a year over 5 year(s) since 2023 |
| Impact for its field and year | 4 / 6 | Cited 12.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 3 / 4 | Cited 80 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Carlos C Cruchaga: h-index 102 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 3 / 3 | OpenAlex lists 10 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 37406134) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 52 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1126/scitranslmed.abq5923
- PubMed: 37406134
- Original source →
- Free full text: IUScholarWorks (Indiana University) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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
Sung, Y. J., Yang, C., Norton, J., Johnson, M., Fagan, A., Bateman, R. J., et al. (2023). Proteomics of brain, CSF, and plasma identifies molecular signatures for distinguishing sporadic and genetic Alzheimer's disease. Science translational medicine. https://doi.org/10.1126/scitranslmed.abq5923
Vancouver
Sung YJ, Yang C, Norton J, Johnson M, Fagan A, Bateman RJ, et al. Proteomics of brain, CSF, and plasma identifies molecular signatures for distinguishing sporadic and genetic Alzheimer's disease. Science translational medicine. 2023. doi:10.1126/scitranslmed.abq5923. PMID: 37406134.
BibTeX
@article{sung2023-37406134,
author = {Sung, Y. J. and Yang, C. and Norton, J. and Johnson, M. and Fagan, A. and Bateman, R. J. and Perrin, R. J. and Morris, J. C. and others},
title = {{Proteomics of brain, CSF, and plasma identifies molecular signatures for distinguishing sporadic and genetic Alzheimer's disease}},
journal = {Science translational medicine},
year = {2023},
doi = {10.1126/scitranslmed.abq5923},
pmid = {37406134},
url = {https://doi.org/10.1126/scitranslmed.abq5923}
}
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