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Genomics of Alzheimer Disease: A Review
Rosenberg RN, Lambracht-Washington D, Yu G, Xia W.. JAMA neurology, 2016-07-01
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Importance To provide a comprehensive review of knowledge of the genomics of Alzheimer disease (AD) and DNA amyloid β 42 (Aβ42) vaccination as a potential therapy. Observations Genotype-phenotype correlations of AD are presented to provide a comprehensive appreciation of the spectrum of disease causation. Alzheimer disease is caused in part by the overproduction and lack of clearance of Aβ protein.
What this study adds
Evidence grade: Low
This is a narrative review. This review covers the genomics of Alzheimer's disease and discusses DNA amyloid beta 42 vaccination as a potential therapy. It is a review of existing knowledge and does not report that any vaccine or genetic treatment works in patients.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Rosenberg, R. N., Lambracht-Washington, D., Yu, G., & Xia, W. (2016). Genomics of Alzheimer Disease: A Review. JAMA neurology. https://doi.org/10.1001/jamaneurol.2016.0301
Vancouver
Rosenberg RN, Lambracht-Washington D, Yu G, Xia W. Genomics of Alzheimer Disease: A Review. JAMA neurology. 2016. doi:10.1001/jamaneurol.2016.0301. PMID: 27135718.
BibTeX
@article{rosenberg2016-27135718,
author = {Rosenberg, R. N. and Lambracht-Washington, D. and Yu, G. and Xia, W.},
title = {{Genomics of Alzheimer Disease: A Review}},
journal = {JAMA neurology},
year = {2016},
doi = {10.1001/jamaneurol.2016.0301},
pmid = {27135718},
url = {https://doi.org/10.1001/jamaneurol.2016.0301}
}
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
- Observations Genotype-phenotype correlations of AD are presented to provide a comprehensive appreciation of the spectrum of disease causation.
- Alzheimer disease is caused in part by the overproduction and lack of clearance of Aβ protein.
- Oligomer Aβ, the most toxic species of Aβ, causes direct injury to neurons, accompanied by enhanced neuroinflammation, astrocytosis and gliosis, and eventually neuronal loss.
- The strongest genetic evidence supporting this hypothesis derives from mutations in the amyloid precursor protein (APP) gene.
Why it matters
This review covers the genomics of Alzheimer's disease and discusses DNA amyloid beta 42 vaccination as a potential therapy. It is a review of existing knowledge and does not report that any vaccine or genetic treatment works in patients.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 45/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (JAMA neurology) |
| Journal's citation record | 2 / 4 | JAMA Neurology: journal h-index 235 (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 | 2016 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 146 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.2 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 4 / 6 | Cited 10.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 2 / 4 | Cited 37 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Weiming Xia: h-index 57 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Boston University: institution h-index 1,456 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27135718) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1001/jamaneurol.2016.0301
- PubMed: 27135718
- Original source →
- Free full text: PubMed Central →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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