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, 2012]. This would, in combination with previously reported findings, support a continuum model of neuropsychiatric disease such as proposed by Craddock et al. [2010]. In this model, the psychiatric phenotypes are ordered along a gradient of decreasing neurodevelopmental impairment, starting with mental retardation, then through autism, schizophrenia, and bipolar disorder, ending with unipolar mood disorders [Craddock & Owen, 2010]. The data from CNV studies suggest that higher impact Transducin rare genetic variants are more likely to lead to the more severe phenotypes, that is, mental retardation, autism, and schizophrenia. Our results support the complementary assertion as well, that the role of common risk variants may be more prominent for the traits at the milder end of the same spectrum OTX015 supplier (Fig. 2). One possible explanation would be that fecundity is most reduced in the more severe disorders, thus preventing genetic risk variants from becoming common in the population. It is entirely possible that a proportion of autistic children in the AGP collection will develop schizophrenia later in life. Theoretically, this subgroup could be expected to carry more risk alleles that are also included in the schizophrenia polygenic risk score. In turn, one would expect that this group would upwardly bias these variance estimates, thereby explaining more of the variance in the ASD group due to clinical misclassification in these individuals who have yet to develop schizophrenia. However, the lack of discernible variance explained in Selleck BTK inhibitor these analyses may preclude these assumptions and reflect that there is both negligible shared genetic liability based on common variants between the disorders and a negligible proportion of this cohort that shares liability through misclassification in these individuals. This study has several strengths and limitations: the relatively large study sample can be considered a strength, with the number of subjects exceeding the sample sizes of the original studies on polygenic score in schizophrenia which were sufficiently powered to detect significantly explained variance of