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A Microglial Signature Directing Human Aging and Neurodegeneration-Related Gene Networks
Mukherjee S, Klaus C, Pricop-Jeckstadt M, Miller JA, Struebing FL.. Frontiers in neuroscience, 2019-01-24
Topic: Brain proteins, microglia and lab models
Aging is regarded as a major risk factor for neurodegenerative diseases. Thus, a better understanding of the similarities between the aging process and neurodegenerative diseases at the cellular and molecular level may reveal better understanding of this detrimental relationship. In the present study, we mined publicly available gene expression datasets from healthy individuals and patients affected by neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and Huntington's disease) across a broad age spectrum and compared those with mouse aging and mouse cell-type specific gene expression profiles.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mukherjee, S., Klaus, C., Pricop-Jeckstadt, M., Miller, J. A., & Struebing, F. L. (2019). A Microglial Signature Directing Human Aging and Neurodegeneration-Related Gene Networks. Frontiers in neuroscience. https://doi.org/10.3389/fnins.2019.00002
Vancouver
Mukherjee S, Klaus C, Pricop-Jeckstadt M, Miller JA, Struebing FL. A Microglial Signature Directing Human Aging and Neurodegeneration-Related Gene Networks. Frontiers in neuroscience. 2019. doi:10.3389/fnins.2019.00002. PMID: 30733664.
BibTeX
@article{mukherjee2019-30733664,
author = {Mukherjee, S. and Klaus, C. and Pricop-Jeckstadt, M. and Miller, J. A. and Struebing, F. L.},
title = {{A Microglial Signature Directing Human Aging and Neurodegeneration-Related Gene Networks}},
journal = {Frontiers in neuroscience},
year = {2019},
doi = {10.3389/fnins.2019.00002},
pmid = {30733664},
url = {https://doi.org/10.3389/fnins.2019.00002}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Thus, a better understanding of the similarities between the aging process and neurodegenerative diseases at the cellular and molecular level may reveal better understanding of this detrimental relationship.
- In the present study, we mined publicly available gene expression datasets from healthy individuals and patients affected by neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and Huntington's disease) across a broad age spectrum and compared those with mouse aging and mouse cell-type specific gene expression profiles.
- We performed weighted gene co-expression network analysis (WGCNA) and found a gene network strongly related with both aging and neurodegenerative diseases.
- This network was significantly enriched with a microglial signature as imputed from cell type-specific sequencing data.
Why it matters
This work compared existing gene expression datasets from healthy people and people with neurodegenerative diseases, including Alzheimer's, with mouse aging and cell-type data. It is an analysis of existing data and does not test any treatment, so it cannot show whether Alzheimer's can be treated, cured or prevented.
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Study details
- Evidence strengthLow
How this study scored 42/100
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 (Frontiers in neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Neuroscience: journal h-index 226 (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 | 2019 — 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 71 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.9 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 3 / 6 | Cited 4.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Felix L. Struebing: h-index 15 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, Los Angeles: institution h-index 1,923 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 9 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30733664) |
| Free to read | 2 / 2 | Free to read |
| Total | 42 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fnins.2019.00002
- PubMed: 30733664
- Original source →
- Free full text: Frontiers in Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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