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Genetic Risk as a Marker of Amyloid-β and Tau Burden in Cerebrospinal Fluid
Nicola Voyle, Hamel Patel, Amos Folarin, Stephen Newhouse, Caroline Johnston, Pieter Jelle Visser, Richard J B Dobson, Steven J Kiddle et al.. Journal of Alzheimer's disease : JAD, 2017
Topic: Plasma and spinal-fluid biomarkers
In EDAR and DESCRIPA test data, inclusion of a case/control PGRS was no more predictive of Aβ, and a combined Aβ and tau endpoint than the basic models (accuracies of 66.0%, and 73.3% respectively). The tau model saw a small increase in accuracy compared to basic models (59.6%). ADNI 2 test data also showed a slight increase in accuracy for the Aβ model when compared to the basic models (61.4%). We see some evidence that a case/control PGRS is marginally more predictive of Aβ and tau pathology than the basic models. The search for predictive factors of Aβ and tau pathologies, above and beyond demographic information, is still ongoing. Better understanding of AD risk alleles, development of more sensitive assays, and studies of larger sample size are three avenues that may provide such factors. However, the clinical utility of possible predictors of brain Aβ and tau pathologies must also be investigated.*'Beta amyloid oligomers in the early diagnosis of AD and as marker for treatment response'**'Development of screening guidelines and criteria for pre-dementia Alzheimer's disease'.
Key findings
- In EDAR and DESCRIPA test data, inclusion of a case/control PGRS was no more predictive of Aβ, and a combined Aβ and tau endpoint than the basic models (accuracies of 66.0%, and 73.3% respectively).
- The tau model saw a small increase in accuracy compared to basic models (59.6%).
- ADNI 2 test data also showed a slight increase in accuracy for the Aβ model when compared to the basic models (61.4%).
- We see some evidence that a case/control PGRS is marginally more predictive of Aβ and tau pathology than the basic models.
- The search for predictive factors of Aβ and tau pathologies, above and beyond demographic information, is still ongoing.
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Study details
- Effect size66.0%; 73.3%; 59.6%
- Evidence strengthLow
How this study scored 43/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 24 of the 56 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of Alzheimer's disease : JAD) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2017 — 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 | 2 / 3 | Effect reported as a number, without an interval or test |
| 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27834776) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 24 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 24 of the 56 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
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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
Voyle, N., Patel, H., Folarin, A., Newhouse, S., Johnston, C., Visser, P. J., et al. (2017). Genetic Risk as a Marker of Amyloid-β and Tau Burden in Cerebrospinal Fluid. Journal of Alzheimer's disease : JAD. https://doi.org/10.3233/jad-160707
Vancouver
Voyle N, Patel H, Folarin A, Newhouse S, Johnston C, Visser PJ, et al. Genetic Risk as a Marker of Amyloid-β and Tau Burden in Cerebrospinal Fluid. Journal of Alzheimer's disease : JAD. 2017. doi:10.3233/jad-160707. PMID: 27834776.
BibTeX
@article{voyle2017-27834776,
author = {Voyle, Nicola and Patel, Hamel and Folarin, Amos and Newhouse, Stephen and Johnston, Caroline and Visser, Pieter Jelle and Dobson, Richard J B and Kiddle, Steven J and others},
title = {{Genetic Risk as a Marker of Amyloid-β and Tau Burden in Cerebrospinal Fluid}},
journal = {Journal of Alzheimer's disease : JAD},
year = {2017},
doi = {10.3233/jad-160707},
pmid = {27834776},
url = {https://doi.org/10.3233/jad-160707}
}