ArticleAnnals of neurology2010
What role for genetics in the prediction of multiple sclerosis?
Article in Annals of neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- Multiple Sclerosis Polygenic Risk Is Not Enriched in Three Multicase Families in Comparison to Population-Based Cases.Human mutation · 2024Article
- Prediction of treatment response in rheumatoid arthritis patients using genome-wide SNP data.Genetic epidemiology · 2018Article
- Multiple sclerosis risk loci correlate with cervical cord atrophy and may explain the course of disability.Neurogenetics · 2015Article
- Combinations of susceptibility genes are associated with higher risk for multiple sclerosis and imply disease course specificity.PloS one · 2015Article
- Noise in multiple sclerosis: unwanted and necessary.Annals of clinical and translational neurology · 2014Article
- Genetic burden in multiple sclerosis families.Genes and immunity · 2013Article
- Power and predictive accuracy of polygenic risk scores.PLoS genetics · 2013Article
- Progress in multiple sclerosis genetics.Current genomics · 2012Article
- [The genetic profile of multiple sclerosis: risk genes and the "dark matter"].Der Nervenarzt · 2012Review
- Multiple sclerosis.The Journal of clinical investigation · 2012Review
- The immunogenetic architecture of autoimmune disease.Cold Spring Harbor perspectives in biology · 2012Review
- The problems and promises of research into human immunology and autoimmune disease.Nature medicine · 2012Article
- Genomic medicine and neurological disease.Human genetics · 2011Review
- Modeling the cumulative genetic risk for multiple sclerosis from genome-wide association data.Genome medicine · 2011Article
- Varicella zoster virus and relapsing remitting multiple sclerosis.Multiple sclerosis international · 2011Article
- Article
- Aggregation of multiple sclerosis genetic risk variants in multiple and single case families.Annals of neurology · 2011Article
- Multiple sclerosis genetics--is the glass half full, or half empty?Nature reviews. Neurology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
For most of us, the foundations of our understanding of genetics were laid by considering Mendelian diseases in which familial recurrence risks are high, and mutant alleles are both necessary and sufficient. One consequence of this deterministic teaching is that our conceptualization of genetics tends to be dominated by the notion that the genetic aspects of disease are caused by rare alleles exerting large effects. Unfortunately, the preconceptions that flow from this training are frequently erroneous and misleading in the context of common traits, where familial recurrence risks are modest, and for the most part the relevant alleles are neither rare, necessary, nor sufficient. For these common traits, the genetic architecture is far more complex, with susceptibility rather than causality resulting from the combined effects of many alleles, each exerting only a modest effect on risk. None of these alleles is sufficient to cause disease on its own, and none is essential for the development of disease. Furthermore, most are carried by large sections of the population, the vast majority of which does not develop the disease. One consequence of our innate belief in the Mendelian paradigm is that we have an inherent expectation that knowledge about the genetic basis for a disease should allow genetic testing and thereby accurate risk prediction. There is an inevitable feeling that the same should be true in complex disease, but is it?
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.