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Manolio, T.A. et al. Finding the missing heritability of complex diseases.
Manolio, T. A. et al. Finding the missing heritability of complex diseases.
Next-generation sequencing (NGS) in family-based study designs will be pivotal in unlocking the missing heritability of common complex diseases.
The missing heritability of polygenic schizophrenia after genome-wide association studies (GWAS) can be potentially accounted for by the fact that most dynamic multiallelic copy number variants (CNVs) overlap segmental duplications (SDs).
This provides an alternative framework to explain the missing heritability of complex traits.
Interactions between variants may contribute to the missing heritability of complex traits.
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Given the 'missing heritability' of human AIDs, and the fact that current GWAS have captured primarily common genetic SNP variants, it is likely that rare or structural variants explain much of the missing heritability, the identification of which will require new and emerging technologies.
Models that consider epistasis, or the interaction between genetic variants, may explain the some of the "missing-heritability" of complex traits [ 1, 2].
In aggregate, such findings have led to the notion that epigenetic factors may be relevant to complex non-Mendelian phenotypes like BD (Labrie et al. 2012; Petronis 2003) and may account for a fraction of the 'missing heritability' of complex traits (Maher 2008).
> -wrap-foot> Explaining this 'missing heritability' of complex diseases (11– 13) is an area of active research, and there are likely to be multiple contributing factors.
The identification of multiple signals at individual loci could explain additional phenotypic variance ('missing heritability') of common traits, and help identify causal genes.
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