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Genetic association studies have identified many candidate genes for human intelligence; however, many candidates fail to be replicated between studies and populations (4).
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SNPs in a number of genomic regions have recently been associated with human stature, but similar to the linkage analysis, few findings have been replicated between studies [2] [4].
The distribution of changes has been replicated between studies [ 2], and may be considered a 'structural signature' of schizophrenia within the brain.
Many of the regions in CNV databases today will prove to be false discoveries, particularly loci that have not been validated independently or are not replicated between studies [25].
These sex-specific relations between work environmental factors and MDD need to be replicated by future studies.
These findings should be replicated in future studies and the relationship between the soluble Aβ and Aβ sequestered in plaques, and also other processes, such as reactive gliosis and inflammatory responses should be systematically evaluated in order to elucidate further the relationship between amyloid-β and cognition at the early stage of plaque formation.
However, very few markers have been replicated consistently between studies.
These represent approximately 240 genes, but unfortunately most are not replicated between studies [ 50, 51].
Overall, these results need to be replicated due to disagreement between studies, although a recent meta-analysis of plasma core biomarkers in AD indicates that Aβ1-42/Aβ1-40 predicto progression to dementia [ 29].
Interestingly, the association between PLD3 and LOAD was largely driven by variants not significantly associated with the phenotype in the original study,11 whereas the individual variants showing significant associations in the original study could be replicated directly.
It called for the study to be replicated in children.
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