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Comment & Response |

Family-Based Replication Study of Schizophrenia Genes

Karolina A. Aberg, PhD1; Edwin J. C. G. van den Oord, PhD1
[+] Author Affiliations
1Center for Biomarker Research and Personalized Medicine, Virginia Commonwealth University, Richmond
JAMA Psychiatry. 2014;71(10):1195-1196. doi:10.1001/jamapsychiatry.2014.375.
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To the Editor In response to our family-based replication study of schizophrenia genes,1 Lazzeroni2 expressed concerns regarding the interpretation of the replication results and argued that simpler studies may ultimately yield faster progress in psychiatric genetics.

We presented 4 arguments that speak to the replication status of our results: (1) the highly significant enrichment of single-nucleotide polymorphisms (SNPs) with small P values in the replication; (2) an 89% to 93% agreement between the direction of effects in our case-control genome-wide association study meta-analysis used to select SNPs and the SNPs that replicated; (3) several findings that replicated across ancestral groups; and (4) replicating SNPs were organized in meaningful biological patterns. Lazzeroni2 focused mainly on the second argument. Based on a simulation study involving 800 unrelated cases and control individuals, she suggested that odds ratios greater than 1 may be enriched among the top results (even if none of the SNPs have an effect) and that this artifact could potentially have caused the high agreement in our study. On behalf of the Family-Based Replication Consortium, we have 2 responses.

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