Imperial College London

ProfessorMarjo-RiittaJarvelin

Faculty of MedicineSchool of Public Health

Chair in Lifecourse Epidemiology
 
 
 
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Contact

 

m.jarvelin

 
 
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Location

 

302School of Public HealthWhite City Campus

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Summary

 

Publications

Citation

BibTex format

@article{Gormley:2018:10.1016/j.neuron.2018.04.014,
author = {Gormley, P and Kurki, MI and Hiekkala, ME and Veerapen, K and Häppölä, P and Mitchell, AA and Lal, D and Palta, P and Surakka, I and Kaunisto, MA and Hämäläinen, E and Vepsäläinen, S and Havanka, H and Harno, H and Ilmavirta, M and Nissilä, M and Säkö, E and Sumelahti, M-L and Liukkonen, J and Sillanpää, M and Metsähonkala, L and Koskinen, S and Lehtimäki, T and Raitakari, O and Männikkö, M and Ran, C and Belin, AC and Jousilahti, P and Anttila, V and Salomaa, V and Artto, V and Färkkilä, M and 23andMe, Research Team and International, Headache Genetics Consortium IHGC and Runz, H and Daly, MJ and Neale, BM and Ripatti, S and Kallela, M and Wessman, M and Palotie, A},
doi = {10.1016/j.neuron.2018.04.014},
journal = {Neuron},
pages = {743--753.e4},
title = {Common variant burden contributes to the familial aggregation of migraine in 1,589 families},
url = {http://dx.doi.org/10.1016/j.neuron.2018.04.014},
volume = {98},
year = {2018}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Complex traits, including migraine, often aggregate in families, but the underlying genetic architecture behind this is not well understood. The aggregation could be explained by rare, penetrant variants that segregate according to Mendelian inheritance or by the sufficient polygenic accumulation of common variants, each with an individually small effect, or a combination of the two hypotheses. In 8,319 individuals across 1,589 migraine families, we calculated migraine polygenic risk scores (PRS) and found a significantly higher common variant burden in familial cases (n = 5,317, OR = 1.76, 95% CI = 1.71-1.81, p = 1.7 × 10-109) compared to population cases from the FINRISK cohort (n = 1,101, OR = 1.32, 95% CI = 1.25-1.38, p = 7.2 × 10-17). The PRS explained 1.6% of the phenotypic variance in the population cases and 3.5% in the familial cases (including 2.9% for migraine without aura, 5.5% for migraine with typical aura, and 8.2% for hemiplegic migraine). The results demonstrate a significant contribution of common polygenic variation to the familial aggregation of migraine.
AU - Gormley,P
AU - Kurki,MI
AU - Hiekkala,ME
AU - Veerapen,K
AU - Häppölä,P
AU - Mitchell,AA
AU - Lal,D
AU - Palta,P
AU - Surakka,I
AU - Kaunisto,MA
AU - Hämäläinen,E
AU - Vepsäläinen,S
AU - Havanka,H
AU - Harno,H
AU - Ilmavirta,M
AU - Nissilä,M
AU - Säkö,E
AU - Sumelahti,M-L
AU - Liukkonen,J
AU - Sillanpää,M
AU - Metsähonkala,L
AU - Koskinen,S
AU - Lehtimäki,T
AU - Raitakari,O
AU - Männikkö,M
AU - Ran,C
AU - Belin,AC
AU - Jousilahti,P
AU - Anttila,V
AU - Salomaa,V
AU - Artto,V
AU - Färkkilä,M
AU - 23andMe,Research Team
AU - International,Headache Genetics Consortium IHGC
AU - Runz,H
AU - Daly,MJ
AU - Neale,BM
AU - Ripatti,S
AU - Kallela,M
AU - Wessman,M
AU - Palotie,A
DO - 10.1016/j.neuron.2018.04.014
EP - 753
PY - 2018///
SN - 0896-6273
SP - 743
TI - Common variant burden contributes to the familial aggregation of migraine in 1,589 families
T2 - Neuron
UR - http://dx.doi.org/10.1016/j.neuron.2018.04.014
UR - https://www.ncbi.nlm.nih.gov/pubmed/29731251
UR - http://hdl.handle.net/10044/1/60715
VL - 98
ER -