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However, we are still some way from finding the molecular variants that explain the heritability of the trait.
Until recently, there had been limited success in identifying the specific genetic variants that explain normal variation of human height.
No genetic variants that significantly contribute to personality variation were identified, while our sample provides over 90% power to detect variants that explain only 1% of the trait variance.
The aims of this study were to elucidate the influence of common genetic variants on childhood attention-deficit/hyperactivity disorder (ADHD) symptoms, to identify genetic variants that explain its high heritability, and to investigate the genetic overlap of ADHD symptom scores with ADHD diagnosis.
Therefore it is not expected that there is a simple explanation with an obvious candidate gene but it is more likely a network of genes and intragenic variants that explain the variation of these traits.
Therefore it is not expected that there is a simple explanation with an obvious candidate gene, it is more likely a network of genes and intragenic variants that explain the variation of these traits.
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We performed low-pass whole-genome sequencing in 680 individuals from the InCHIANTI study to test two primary hypotheses: (i) that sequencing would detect single low-frequency large effect variants that explow-frequency largents of pheffectic variants as single common varianthatand (ii) that somexplainedvariant asimilarions could be explamountsy lof-frequency variants.
Fine-mapping methods take as input the full set of association signals in a region and attempt to identify a minimum set of variants that explains the association signals.
We had adequate power to detect a variant that explained even 2.5% of the variation in cigarettes per day.
For example, if a sample size of N≈780 is required for a power of 80% to detect a genetic variant that explains 1% of the variance in the error-free latent trait, then N≈1300 is required to achieve the same power if the psychometric instrument has a reliability of.7.
There are ∼35 known single-nucleotide variants (SNVs) that explain only ∼10% of variation in triglyceride (TG) level.
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