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Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways
Rosenthal SL, Kamboh MI.. Current genetic medicine reports, 2014-03-22
Topic: Amyloid, tau and blood-test diagnosis
Late-onset Alzheimer's disease (LOAD) is a devastating neurodegenerative disease with no effective treatment or cure. In addition to APOE , recent large genome-wide association studies have identified variation in over 20 loci that contribute to disease risk: CR1, BIN1, INPP5D, MEF2C, TREM2, CD2AP, HLA - DRB1/HLA - DRB5, EPHA1, NME8, ZCWPW1, CLU, PTK2B, PICALM, SORL1, CELF1, MS4A4/MS4A6E, SLC24A4/RIN3,FERMT2, CD33, ABCA7, CASS4 . In addition, rare variants associated with LOAD have also been identified in APP , TREM2 and PLD3 genes.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Rosenthal, S. L., & Kamboh, M. I. (2014). Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways. Current genetic medicine reports. https://doi.org/10.1007/s40142-014-0034-x
Vancouver
Rosenthal SL, Kamboh MI. Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways. Current genetic medicine reports. 2014. doi:10.1007/s40142-014-0034-x. PMID: 24829845.
BibTeX
@article{rosenthal2014-24829845,
author = {Rosenthal, S. L. and Kamboh, M. I.},
title = {{Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways}},
journal = {Current genetic medicine reports},
year = {2014},
doi = {10.1007/s40142-014-0034-x},
pmid = {24829845},
url = {https://doi.org/10.1007/s40142-014-0034-x}
}
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
- In addition to APOE , recent large genome-wide association studies have identified variation in over 20 loci that contribute to disease risk: CR1, BIN1, INPP5D, MEF2C, TREM2, CD2AP, HLA - DRB1/HLA - DRB5, EPHA1, NME8, ZCWPW1, CLU, PTK2B, PICALM, SORL1, CELF1, MS4A4/MS4A6E, SLC24A4/RIN3,FERMT2, CD33, ABCA7, CASS4 .
- In addition, rare variants associated with LOAD have also been identified in APP , TREM2 and PLD3 genes.
- Previous research has identified inflammatory response, lipid metabolism and homeostasis, and endocytosis as the likely modes through which these gene products participate in Alzheimer's disease.
- Despite the clustering of these genes across a few common pathways, many of their roles in disease pathogenesis have yet to be determined.
Why it matters
This review lists over 20 gene regions, plus rare variants in APP, TREM2 and PLD3, that contribute to late-onset Alzheimer's disease risk. It notes there is still no effective treatment or cure, so these genetic findings are leads for research rather than therapies.
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 (Current genetic medicine reports) |
| Journal's citation record | 0 / 4 | Current Genetic Medicine Reports: journal h-index 34 (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 | 2014 — within 20 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 | 5 / 7 | Cited 154 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.0 citations a year over 14 year(s) since 2014 |
| Impact for its field and year | 4 / 6 | Cited 11.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 2 / 4 | Cited 19 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author M. Ilyas Kamboh: h-index 83 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Pittsburgh: institution h-index 1,470 (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 24829845) |
| Free to read | 2 / 2 | Free to read |
| Total | 43 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1007/s40142-014-0034-x
- PubMed: 24829845
- Original source →
- Free full text: Current Genetic Medicine Reports →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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