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M

Manuel A. R. Ferreira

Researcher at QIMR Berghofer Medical Research Institute

Publications -  163
Citations -  50023

Manuel A. R. Ferreira is an academic researcher from QIMR Berghofer Medical Research Institute. The author has contributed to research in topics: Genome-wide association study & Single-nucleotide polymorphism. The author has an hindex of 53, co-authored 137 publications receiving 42268 citations. Previous affiliations of Manuel A. R. Ferreira include Broad Institute & Royal Brisbane and Women's Hospital.

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PLINK: A Tool Set for Whole-Genome Association and Population-Based Linkage Analyses

TL;DR: This work introduces PLINK, an open-source C/C++ WGAS tool set, and describes the five main domains of function: data management, summary statistics, population stratification, association analysis, and identity-by-descent estimation, which focuses on the estimation and use of identity- by-state and identity/descent information in the context of population-based whole-genome studies.
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Common polygenic variation contributes to risk of schizophrenia and bipolar disorder

Shaun Purcell, +81 more
- 06 Aug 2009 - 
TL;DR: The extent to which common genetic variation underlies the risk of schizophrenia is shown, using two analytic approaches, and the major histocompatibility complex is implicate, which is shown to involve thousands of common alleles of very small effect.
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Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4

Pamela Sklar, +192 more
- 01 Oct 2011 - 
TL;DR: An analysis of all 11,974 bipolar disorder cases and 51,792 controls confirmed genome-wide significant evidence of association for CACNA1C and identified a new intronic variant in ODZ4, and a pathway comprised of subunits of calcium channels enriched in bipolar disorder association intervals was identified.
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Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder

TL;DR: The results suggest that ion channelopathies may be involved in the pathogenesis of bipolar disorder and found further support for the previously reported CACNA1C.