Forskning
Udskriv Udskriv
Switch language
Rigshospitalet - en del af Københavns Universitetshospital
Udgivet

Mendelian randomization implies no direct causal association between leukocyte telomere length and amyotrophic lateral sclerosis

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Infants with congenital heart defects have reduced brain volumes

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. De novo electrocardiographic abnormalities in persons living with HIV

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Using machine learning for predicting intensive care unit resource use during the COVID-19 pandemic in Denmark

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Effect of liraglutide on expression of inflammatory genes in type 2 diabetes

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. CCG•CGG interruptions in high-penetrance SCA8 families increase RAN translation and protein toxicity

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Endophenotypical drift in Huntington's disease: a 5-year follow-up study

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

We employed Mendelian randomization (MR) to evaluate the causal relationship between leukocyte telomere length (LTL) and amyotrophic lateral sclerosis (ALS) with summary statistics from genome-wide association studies (n = ~ 38,000 for LTL and ~ 81,000 for ALS in the European population; n = ~ 23,000 for LTL and ~ 4,100 for ALS in the Asian population). We further evaluated mediation roles of lipids in the pathway from LTL to ALS. The odds ratio per standard deviation decrease of LTL on ALS was 1.10 (95% CI 0.93-1.31, p = 0.274) in the European population and 0.75 (95% CI 0.53-1.07, p = 0.116) in the Asian population. This null association was also detected between LTL and frontotemporal dementia in the European population. However, we found that an indirect effect of LTL on ALS might be mediated by low density lipoprotein (LDL) or total cholesterol (TC) in the European population. These results were robust against extensive sensitivity analyses. Overall, our MR study did not support the direct causal association between LTL and the ALS risk in neither population, but provided suggestive evidence for the mediation role of LDL or TC on the influence of LTL and ALS in the European population.

OriginalsprogEngelsk
Artikelnummer12184
TidsskriftScientific Reports
Vol/bind10
Udgave nummer1
Sider (fra-til)12184
ISSN2045-2322
DOI
StatusUdgivet - 1 dec. 2020

ID: 61265271