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Cruchaga & Goate reply

Nature volume 520, pages E5–E6 (2015)Cite this article

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replying to J.-C. Lambert et al. Nature 520, 10.1038/nature14036 (2015); S. J. van der Lee et al. Nature 520, 10.1038/nature14038 (2015); S. Heilmann et al. Nature 520, 10.1038/nature14039 (2015)

In a recent study we used a family-based study design followed by custom genotyping and sequencing in large case–control data sets. We found that several low-frequency variants, including Val232Met, in PLD3 were enriched in Alzheimer's disease cases compared to controls1. van der Lee et al.2, Heilmann et al.3 and Lambert et al.4 independently attempted to replicate the association between the Val232Met variant and Alzheimer's disease risk in case–control data sets, population cohorts and family-based studies.

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References

  1. Cruchaga, C. et al. Rare coding variants in the phospholipase D3 gene confer risk for Alzheimer's disease. Nature 505, 550–554 (2014)

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  2. van der Lee, S. J. et al. PLD3 variants in population studies. Nature 520, http://dx.doi.org/10.1038/nature14038 (2015).

  3. Heilmann, S. et al. PLD3 in non-familial Alzheimer's disease. Nature 520, http://dx.doi.org/10.1038/nature14039 (2015).

  4. Lambert, J.-C. et al. PLD3 and sporadic Alzheimer's disease risk. Nature 520, http://dx.doi.org/10.1038/nature14036 (2015).

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Authors and Affiliations

  1. Department of Psychiatry, Washington University, St Louis, 63110, Missouri, USA

    Carlos Cruchaga & Alison M. Goate

  2. Hope Center Program on Protein Aggregation and Neurodegeneration, Washington University St Louis, Missouri, 63110, USA

    Carlos Cruchaga & Alison M. Goate

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  1. Carlos Cruchaga
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  2. Alison M. Goate
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Correspondence to Carlos Cruchaga.

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Cruchaga, C., Goate, A. Cruchaga & Goate reply. Nature 520, E5–E6 (2015). https://doi.org/10.1038/nature14037

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