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Genome-wide RNAseq study of the molecular mechanisms underlying microglia activation in response to pathological tau perturbation in the rTg4510 tau transgenic animal model
Wang H, Li Y, Ryder JW, Hole JT, Ebert PJ, Airey DC, Qian HR, Logsdon B et al.. Molecular neurodegeneration, 2018-12-17
Topic: Brain proteins, microglia and lab models
Background Activation of microglia, the resident immune cells of the central nervous system, is a prominent pathological hallmark of Alzheimer's disease (AD). However, the gene expression changes underlying microglia activation in response to tau pathology remain elusive. Furthermore, it is not clear how murine gene expression changes relate to human gene expression networks.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wang, H., Li, Y., Ryder, J. W., Hole, J. T., Ebert, P. J., Airey, D. C., et al. (2018). Genome-wide RNAseq study of the molecular mechanisms underlying microglia activation in response to pathological tau perturbation in the rTg4510 tau transgenic animal model. Molecular neurodegeneration. https://doi.org/10.1186/s13024-018-0296-y
Vancouver
Wang H, Li Y, Ryder JW, Hole JT, Ebert PJ, Airey DC, et al. Genome-wide RNAseq study of the molecular mechanisms underlying microglia activation in response to pathological tau perturbation in the rTg4510 tau transgenic animal model. Molecular neurodegeneration. 2018. doi:10.1186/s13024-018-0296-y. PMID: 30558641.
BibTeX
@article{wang2018-30558641,
author = {Wang, H. and Li, Y. and Ryder, J. W. and Hole, J. T. and Ebert, P. J. and Airey, D. C. and Qian, H. R. and Logsdon, B. and others},
title = {{Genome-wide RNAseq study of the molecular mechanisms underlying microglia activation in response to pathological tau perturbation in the rTg4510 tau transgenic animal model}},
journal = {Molecular neurodegeneration},
year = {2018},
doi = {10.1186/s13024-018-0296-y},
pmid = {30558641},
url = {https://doi.org/10.1186/s13024-018-0296-y}
}
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
- However, the gene expression changes underlying microglia activation in response to tau pathology remain elusive.
- Furthermore, it is not clear how murine gene expression changes relate to human gene expression networks.
- Methods Microglia cells were isolated from rTg4510 tau transgenic mice and gene expression was profiled using RNA sequencing.
- Four age groups of mice (2-, 4-, 6-, and 8-months) were analyzed to capture longitudinal gene expression changes that correspond to varying levels of pathology, from minimal tau accumulation to massive neuronal loss.
Why it matters
This study profiled gene expression in microglia isolated from tau transgenic mice across four age groups to see what changes accompany microglial activation in response to tau pathology. It is animal research only and reports no treatment, cure or prevention for people.
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Study details
- Study designlongitudinal study
- Evidence strengthModerate
How this study scored 54/100
Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for sample size, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular neurodegeneration) |
| Journal's citation record | 2 / 4 | Molecular Neurodegeneration: journal h-index 164 (OpenAlex, 2026-10-29) |
| Study design | 7 / 12 | A longitudinal study following the same people over 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 | 2018 — 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 “transgenic”) — scores zero |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 83 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.3 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 3 / 6 | Cited 4.0× 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 | 2 / 4 | Cited 23 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Ronald Bradley Demattos: h-index 41 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Eli Lilly (United States): institution h-index 744 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30558641) |
| Free to read | 2 / 2 | Free to read |
| Total | 54 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-018-0296-y
- PubMed: 30558641
- Original source →
- Free full text: Molecular Neurodegeneration →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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