Topic: Brain proteins, microglia and lab models
The successful discovery of genes that cause rare monogenic disorders has dominated our understanding of the genetic basis of neurodegenerative disease. The emergence of robust genome-wide association methodologies promises to explain the genetic etiology of the common sporadic forms of complex diseases. In addition to revealing the genetic susceptibility of neurodegenerative disease, genome-wide association studies (GWASs) should also be an unbiased generator of molecules that are relevant in disease pathogenesis. Despite this exciting potential, GWAS results have varied in their consistency and their ability to deliver these aims. The largest challenge that faces neuroscientists is the interpretation of the results of GWASs and the translation of the genetic findings into functional mechanisms that are biologically important in disease pathogenesis and, ultimately, treatment design. We examine recent results from GWASs of Alzheimer's disease and Parkinson's disease and explore their use and limitations. We further reflect on how these results may expedite progress in understanding and influencing the molecular pathogenesis of neurodegeneration.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Gandhi, S., & Wood, N. W. (2010). Genome-wide association studies: the key to unlocking neurodegeneration? Nature neuroscience. https://doi.org/10.1038/nn.2584
Vancouver
Gandhi S, Wood NW. Genome-wide association studies: the key to unlocking neurodegeneration? Nature neuroscience. 2010. doi:10.1038/nn.2584. PMID: 20581814.
BibTeX
@article{gandhi2010-20581814,
author = {Gandhi, S. and Wood, N. W.},
title = {{Genome-wide association studies: the key to unlocking neurodegeneration?}},
journal = {Nature neuroscience},
year = {2010},
doi = {10.1038/nn.2584},
pmid = {20581814},
url = {https://doi.org/10.1038/nn.2584}
}
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Key findings
- Despite this exciting potential, GWAS results have varied in their consistency and their ability to deliver these aims.
- The largest challenge that faces neuroscientists is the interpretation of the results of GWASs and the translation of the genetic findings into functional mechanisms that are biologically important in disease pathogenesis and, ultimately, treatment design.
- We examine recent results from GWASs of Alzheimer's disease and Parkinson's disease and explore their use and limitations.
- We further reflect on how these results may expedite progress in understanding and influencing the molecular pathogenesis of neurodegeneration.
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Study details
- Evidence strengthLow
How this study scored 40/100
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. 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 and multicenter collaboration, so those were left out: it earned 23 of the 58 points we could judge it on, which is 40 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Nature neuroscience) |
| 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 | 1 / 5 | 2010 — 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 | — / 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 |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 20581814) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 23 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 23 of the 58 points we could judge it on is 40 out of 100. |
| Total | 40 / 100 | — |
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