Home › Research › Risk genes beyond APOE
Genetic modulation of senescent phenotypes in Homo sapiens
Martin GM.. Cell, 2005-02-01
Topic: Brain proteins, microglia and lab models
Single-gene mutations can produce human progeroid syndromes--phenotypes that mimic usual or "normative" aging. These can be divided into two classes--those that have their impacts upon multiple organs and tissues (segmental progeroid syndromes) and those that have their major impacts upon a single organ or tissue (unimodal progeroid syndromes). The prototypic example of the former is the Werner syndrome, a condition caused by mutations of the RecQ family of DNA helicases.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Martin, G. M. (2005). Genetic modulation of senescent phenotypes in Homo sapiens. Cell. https://doi.org/10.1016/j.cell.2005.01.031
Vancouver
Martin GM. Genetic modulation of senescent phenotypes in Homo sapiens. Cell. 2005. doi:10.1016/j.cell.2005.01.031. PMID: 15734684.
BibTeX
@article{martin2005-15734684,
author = {Martin, G. M.},
title = {{Genetic modulation of senescent phenotypes in Homo sapiens}},
journal = {Cell},
year = {2005},
doi = {10.1016/j.cell.2005.01.031},
pmid = {15734684},
url = {https://doi.org/10.1016/j.cell.2005.01.031}
}
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
- These can be divided into two classes--those that have their impacts upon multiple organs and tissues (segmental progeroid syndromes) and those that have their major impacts upon a single organ or tissue (unimodal progeroid syndromes).
- The prototypic example of the former is the Werner syndrome, a condition caused by mutations of the RecQ family of DNA helicases.
- Research on the Werner syndrome and a surprising number of other progeroid syndromes support the importance of the maintenance of genomic stability as a partial antidote to aging.
- The prototypic examples of the latter are Alzheimer type dementias.
Why it matters
This review discusses single-gene mutations that cause human progeroid syndromes, such as Werner syndrome, which mimic aspects of aging. It does not report a treatment, cure or prevention for Alzheimer's disease.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 43/100
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 (Cell) |
| Journal's citation record | 4 / 4 | Cell: journal h-index 1,220 (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 | 1 / 5 | 2005 — older than 20 years, still counted |
| 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 | 5 / 7 | Cited 171 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.4 citations a year over 23 year(s) since 2005 |
| Impact for its field and year | 3 / 6 | Cited 4.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 1 / 4 | Cited 5 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author George M. Martin: h-index 75 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | University of Washington: institution h-index 3,540 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 15734684) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 43 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Later studies that cite this one
1 study in the alzhub library lists this one in its references.
Related studies in Risk genes beyond APOE
Also in Risk genes beyond APOE
107 studies in the library are filed under Risk genes beyond APOE with no topic tag they share with another; these are this study's neighbours in a fixed tour of them. The Risk genes beyond APOE hub.