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Genome-wide interaction study of brain beta-amyloid burden and cognitive impairment in Alzheimer's disease
Roostaei T, Nazeri A, Felsky D, De Jager PL, Schneider JA, Pollock BG, Bennett DA, Voineskos AN et al.. Molecular psychiatry, 2016-03-29
Topic: Amyloid, tau and blood-test diagnosis
The lack of strong association between brain beta-amyloid deposition and cognitive impairment has been a challenge for the Alzheimer's disease (AD) field. Although beta-amyloid is necessary for the pathologic diagnosis of AD, it is not sufficient to make the pathologic diagnosis or cause dementia. We sought to identify the genetic modifiers of the relation between cortical beta-amyloid burden (measured using [ 18 F]Florbetapir-PET) and cognitive dysfunction (measured using ADAS-cog) by conducting a genome-wide interaction study on baseline data from participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI) phases GO/2 (n=678).
Key findings
- Although beta-amyloid is necessary for the pathologic diagnosis of AD, it is not sufficient to make the pathologic diagnosis or cause dementia.
- We sought to identify the genetic modifiers of the relation between cortical beta-amyloid burden (measured using [ 18 F]Florbetapir-PET) and cognitive dysfunction (measured using ADAS-cog) by conducting a genome-wide interaction study on baseline data from participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI) phases GO/2 (n=678).
- Near genome-wide significant interaction effect was observed for rs73069071 within the IAPP (amylin) and SLCO1A2 genes (P=6.2 × 10 -8 ).
- Congruent results were found using data from participants followed up from ADNI-1 (P one-tailed =0.028, n=165).
Why it matters
This genome-wide interaction study in 678 Alzheimer's Disease Neuroimaging Initiative participants looked for genetic factors that modify the relationship between brain beta-amyloid burden and cognitive impairment. The authors note that beta-amyloid is necessary for the pathologic diagnosis of Alzheimer's disease but is not sufficient to cause dementia.
Study details
- Study designmeta-analysis
- Participants678
- Evidence strengthHigh
How this study scored 71/100
Published in a leading specialty journal, and it is a meta-analysis pooling many studies. Scored zero for effect reported because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Molecular psychiatry) |
| Journal's citation record | 3 / 4 | Molecular Psychiatry: journal h-index 318 (OpenAlex, 2026-10-29) |
| Study design | 12 / 12 | A meta-analysis pooling many studies |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2017 — within 10 year(s) of the newest study here |
| Sample size | 2 / 4 | 678 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | A review of other studies — randomisation is not credited here |
| Times cited | 4 / 7 | Cited 70 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.4 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 3 / 6 | Cited 6.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 2 / 4 | Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Aristotle N. Voineskos: h-index 67 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27021820) |
| Free to read | 2 / 2 | Free to read |
| Total | 71 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Roostaei, T., Nazeri, A., Felsky, D., De Jager, P. L., Schneider, J. A., Pollock, B. G., et al. (2017). Genome-wide interaction study of brain beta-amyloid burden and cognitive impairment in Alzheimer's disease. Molecular psychiatry. https://doi.org/10.1038/mp.2016.35
Vancouver
Roostaei T, Nazeri A, Felsky D, De Jager PL, Schneider JA, Pollock BG, et al. Genome-wide interaction study of brain beta-amyloid burden and cognitive impairment in Alzheimer's disease. Molecular psychiatry. 2017. doi:10.1038/mp.2016.35. PMID: 27021820.
BibTeX
@article{roostaei2017-27021820,
author = {Roostaei, T. and Nazeri, A. and Felsky, D. and De Jager, P. L. and Schneider, J. A. and Pollock, B. G. and Bennett, D. A. and Voineskos, A. N. and others},
title = {{Genome-wide interaction study of brain beta-amyloid burden and cognitive impairment in Alzheimer's disease}},
journal = {Molecular psychiatry},
year = {2017},
doi = {10.1038/mp.2016.35},
pmid = {27021820},
url = {https://doi.org/10.1038/mp.2016.35}
}
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