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Telomere length as a modifier of age-at-onset in Huntington disease: a two-sample Mendelian randomization study

  • N. Ahmad Aziz
  • Patrick Weydt
Letter to the Editors

Notes

Compliance with ethical standards

Conflicts of interest

Dr Aziz and Dr Weydt report no conflicts of interest.

References

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    GeM-HD Consortium (2015) Identification of genetic factors that modify clinical onset of Huntington’s disease. Cell 162(3):516–526CrossRefGoogle Scholar
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    Kota LN, Bharath S, Purushottam M et al (2015) Reduced telomere length in neurodegenerative disorders may suggest shared biology. J Neuropsychiatry Clin Neurosci 27(2):e92–e96CrossRefPubMedGoogle Scholar
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    Zhan Y, Song C, Karlsson R et al (2015) Telomere length shortening and Alzheimer disease—a Mendelian randomization study. JAMA Neurol 72(10):1202–1203CrossRefPubMedGoogle Scholar
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    Davey Smith G, Hemani G (2014) Mendelian randomization: genetic anchors for causal inference in epidemiological studies. Hum Mol Genet 23(R1):R89–R98CrossRefPubMedPubMedCentralGoogle Scholar
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    Codd V, Nelson CP, Albrecht E et al (2013) Identification of seven loci affecting mean telomere length and their association with disease. Nat Genet 45(4):422–427CrossRefPubMedPubMedCentralGoogle Scholar
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    Hemani G, Zheng J, Wade KH et al (2016) MR-base: a platform for systematic causal inference across the phenome using billions of genetic associations. bioRxiv.  https://doi.org/10.1101/078972 Google Scholar

Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  1. 1.German Centre for Neurodegenerative Diseases (DZNE)BonnGermany
  2. 2.Department of Neurodegenerative Diseases and GerontopsychiatryUniversity of Bonn Medical CentreBonnGermany

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