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Gene co-expression networks identify Trem2 and Tyrobp as major hubs in human APOE expressing mice following traumatic brain injury
Castranio EL, Mounier A, Wolfe CM, Nam KN, Fitz NF, Letronne F, Schug J, Koldamova R et al.. Neurobiology of disease, 2017-05-11
Topic: Brain proteins, microglia and lab models
Traumatic brain injury (TBI) is strongly linked to an increased risk of developing dementia, including chronic traumatic encephalopathy and possibly Alzheimer's disease (AD). APOEε4 allele of human Apolipoprotein E (APOE) gene is the major genetic risk factor for late onset AD and has been associated with chronic traumatic encephalopathy and unfavorable outcome following TBI. To determine if there is an APOE isoform-specific response to TBI we performed controlled cortical impact on 3-month-old mice expressing human APOE3 or APOE4 isoforms.
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APA 7th
Castranio, E. L., Mounier, A., Wolfe, C. M., Nam, K. N., Fitz, N. F., Letronne, F., et al. (2017). Gene co-expression networks identify Trem2 and Tyrobp as major hubs in human APOE expressing mice following traumatic brain injury. Neurobiology of disease. https://doi.org/10.1016/j.nbd.2017.05.006
Vancouver
Castranio EL, Mounier A, Wolfe CM, Nam KN, Fitz NF, Letronne F, et al. Gene co-expression networks identify Trem2 and Tyrobp as major hubs in human APOE expressing mice following traumatic brain injury. Neurobiology of disease. 2017. doi:10.1016/j.nbd.2017.05.006. PMID: 28502803.
BibTeX
@article{castranio2017-28502803,
author = {Castranio, E. L. and Mounier, A. and Wolfe, C. M. and Nam, K. N. and Fitz, N. F. and Letronne, F. and Schug, J. and Koldamova, R. and others},
title = {{Gene co-expression networks identify Trem2 and Tyrobp as major hubs in human APOE expressing mice following traumatic brain injury}},
journal = {Neurobiology of disease},
year = {2017},
doi = {10.1016/j.nbd.2017.05.006},
pmid = {28502803},
url = {https://doi.org/10.1016/j.nbd.2017.05.006}
}
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Key findings
- APOEε4 allele of human Apolipoprotein E (APOE) gene is the major genetic risk factor for late onset AD and has been associated with chronic traumatic encephalopathy and unfavorable outcome following TBI.
- To determine if there is an APOE isoform-specific response to TBI we performed controlled cortical impact on 3-month-old mice expressing human APOE3 or APOE4 isoforms.
- Following injury, we used several behavior paradigms to test for anxiety and learning and found that APOE3 and APOE4 targeted replacement mice demonstrate cognitive impairments following moderate TBI.
- Transcriptional profiling 14days following injury revealed a significant effect of TBI, which was similar in both genotypes.
Why it matters
In mice expressing human APOE3 or APOE4 isoforms after controlled cortical impact, gene co-expression networks identified Trem2 and Tyrobp as major hubs. This is an animal study of traumatic brain injury, so it does not show whether targeting these genes would treat, cure or prevent Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 40/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of disease) |
| Journal's citation record | 2 / 4 | Neurobiology of Disease: journal h-index 225 (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 | Laboratory or animal study (title names “mice”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 56 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.1 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 2 / 6 | Cited 2.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 1 / 4 | Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Iliya M. Lefterov: h-index 34 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Pennsylvania: institution h-index 1,859 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28502803) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 40 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.nbd.2017.05.006
- PubMed: 28502803
- Original source →
- Free full text: Neurobiology of Disease →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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