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A data-driven approach links microglia to pathology and prognosis in amyotrophic lateral sclerosis
Cooper-Knock J, Green C, Altschuler G, Wei W, Bury JJ, Heath PR, Wyles M, Gelsthorpe C et al.. Acta neuropathologica communications, 2017-03-16
Topic: Brain proteins, microglia and lab models
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that lacks a predictive and broadly applicable biomarker. Continued focus on mutation-specific upstream mechanisms has yet to predict disease progression in the clinic. Utilising cellular pathology common to the majority of ALS patients, we implemented an objective transcriptome-driven approach to develop noninvasive prognostic biomarkers for disease progression.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Cooper-Knock, J., Green, C., Altschuler, G., Wei, W., Bury, J. J., Heath, P. R., et al. (2017). A data-driven approach links microglia to pathology and prognosis in amyotrophic lateral sclerosis. Acta neuropathologica communications. https://doi.org/10.1186/s40478-017-0424-x
Vancouver
Cooper-Knock J, Green C, Altschuler G, Wei W, Bury JJ, Heath PR, et al. A data-driven approach links microglia to pathology and prognosis in amyotrophic lateral sclerosis. Acta neuropathologica communications. 2017. doi:10.1186/s40478-017-0424-x. PMID: 28302159.
BibTeX
@article{cooperknock2017-28302159,
author = {Cooper-Knock, J. and Green, C. and Altschuler, G. and Wei, W. and Bury, J. J. and Heath, P. R. and Wyles, M. and Gelsthorpe, C. and others},
title = {{A data-driven approach links microglia to pathology and prognosis in amyotrophic lateral sclerosis}},
journal = {Acta neuropathologica communications},
year = {2017},
doi = {10.1186/s40478-017-0424-x},
pmid = {28302159},
url = {https://doi.org/10.1186/s40478-017-0424-x}
}
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
- Continued focus on mutation-specific upstream mechanisms has yet to predict disease progression in the clinic.
- Utilising cellular pathology common to the majority of ALS patients, we implemented an objective transcriptome-driven approach to develop noninvasive prognostic biomarkers for disease progression.
- Genes expressed in laser captured motor neurons in direct correlation (Spearman rank correlation, p < 0.01) with counts of neuropathology were developed into co-expression network modules.
- Screening modules using three gene sets representing rate of disease progression and upstream genetic association with ALS led to the prioritisation of a single module enriched for immune response to motor neuron degeneration.
Why it matters
This study used a transcriptome-driven approach to develop noninvasive prognostic biomarkers for progression of amyotrophic lateral sclerosis. It is about ALS, not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Study details
- Evidence strengthLow
How this study scored 45/100
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. We have no data on senior author's track record, so that was left out: it earned 43 of the 96 points we could judge it on, which is 45 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Acta neuropathologica communications) |
| Journal's citation record | 1 / 4 | Acta Neuropathologica Communications: journal h-index 129 (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 | 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 80 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.3 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 3 / 6 | Cited 4.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 2 / 4 | Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | OpenAlex's profile for last-listed author Winston Hide holds only 7 work(s), too few to judge a track record — left out of this score |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28302159) |
| Free to read | 2 / 2 | Free to read |
| Points | 43 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 43 of the 96 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s40478-017-0424-x
- PubMed: 28302159
- Original source →
- Free full text: Acta Neuropathologica Communications →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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