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Weiner, Daniel

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Weiner

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Weiner, Daniel

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2017 - 20182

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Author's Publications: search.filters.isAuthorOfPublication.28bc6ac8-e67a-421c-b27c-8561d86745ab

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    Polygenic risk for schizophrenia and measured domains of cognition in individuals with psychosis and controls
    (Nature Publishing Group UK, 2018) Shafee, Rebecca; Nanda, Pranav; Padmanabhan, Jaya; Tandon, Neeraj; Alliey-Rodriguez, Ney; Kalapurakkel, Sreeja; Weiner, Daniel; Gur, Raquel E.; Keefe, Richard S. E.; Hill, Scot K.; Bishop, Jeffrey R.; Clementz, Brett A.; Tamminga, Carol A.; Gershon, Elliot S.; Pearlson, Godfrey D.; Keshavan, Matcheri; Sweeney, John A.; McCarroll, Steven; Robinson, Elise
    Psychotic disorders including schizophrenia are commonly accompanied by cognitive deficits. Recent studies have reported negative genetic correlations between schizophrenia and indicators of cognitive ability such as general intelligence and processing speed. Here we compare the effect of polygenetic risk for schizophrenia (PRSSCZ) on measures that differ in their relationships with psychosis onset: a measure of current cognitive abilities (the Brief Assessment of Cognition in Schizophrenia, BACS) that is greatly reduced in psychotic disorder patients, a measure of premorbid intelligence that is minimally affected by psychosis onset (the Wide-Range Achievement Test, WRAT); and educational attainment (EY), which covaries with both BACS and WRAT. Using genome-wide single nucleotide polymorphism (SNP) data from 314 psychotic and 423 healthy research participants in the Bipolar-Schizophrenia Network for Intermediate Phenotypes (B-SNIP) Consortium, we investigated the association of PRSSCZ with BACS, WRAT, and EY. Among apparently healthy individuals, greater genetic risk for schizophrenia (PRSSCZ) was significantly associated with lower BACS scores (r = −0.17, p = 6.6 × 10−4 at PT = 1 × 10−4), but not with WRAT or EY. Among individuals with psychosis, PRSSCZ did not associate with variations in any of these three phenotypes. We further investigated the association between PRSSCZ and WRAT in more than 4500 healthy subjects from the Philadelphia Neurodevelopmental Cohort. The association was again null (p > 0.3, N = 4511), suggesting that different cognitive phenotypes vary in their etiologic relationship with schizophrenia.
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    Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders
    (2017) Weiner, Daniel; Wigdor, Emilie M.; Ripke, Stephan; Walters, Raymond; Kosmicki, Jack; Grove, Jakob; Samocha, Kaitlin E.; Goldstein, Jacqueline; Okbay, Aysu; Bybjerg-Grauholm, Jonas; Werge, Thomas; Hougaard, David M.; Taylor, Jacob; Skuse, David; Devlin, Bernie; Anney, Richard; Sanders, Stephan J.; Bishop, Somer; Mortensen, Preben Bo; Børglum, Anders D.; Smith, George Davey; Daly, Mark; Robinson, Elise
    Autism spectrum disorder (ASD) risk is influenced by common polygenic and de novo variation. We aimed to clarify the influence of polygenic risk for ASDs and to identify subgroups of ASD cases, including those with strong acting de novo variants, in which polygenic risk is relevant. Using a novel approach called the polygenic transmission disequilibrium test, and data from 6,454 families with a child with ASD, we show that polygenic risk for ASDs, schizophrenia, and greater educational attainment is over transmitted to children with ASDs. These findings hold independent of proband IQ. We find that polygenic variation contributes additively to risk in ASD cases who carry a strong acting de novo variant. Lastly, we show that elements of polygenic risk are independent and differ in their relationship with phenotype. These results confirm that ASDs’ genetic influences are additive and suggest they create risk through at least partially distinct etiologic pathways.