- Paschou, Peristera;
- Yu, Dongmei;
- Gerber, Gloria;
- Evans, Patrick;
- Tsetsos, Fotis;
- Davis, Lea K;
- Karagiannidis, Iordanis;
- Chaponis, Jonathan;
- Gamazon, Eric;
- Mueller‐Vahl, Kirsten;
- Stuhrmann, Manfred;
- Schloegelhofer, Monika;
- Stamenkovic, Mara;
- Hebebrand, Johannes;
- Noethen, Markus;
- Nagy, Peter;
- Barta, Csaba;
- Tarnok, Zsanett;
- Rizzo, Renata;
- Depienne, Christel;
- Worbe, Yulia;
- Hartmann, Andreas;
- Cath, Danielle C;
- Budman, Cathy L;
- Sandor, Paul;
- Barr, Cathy;
- Wolanczyk, Thomas;
- Singer, Harvey;
- Chou, I‐Ching;
- Grados, Marco;
- Posthuma, Danielle;
- Rouleau, Guy A;
- Aschauer, Harald;
- Freimer, Nelson B;
- Pauls, David L;
- Cox, Nancy J;
- Mathews, Carol A;
- Scharf, Jeremiah M
Tourette syndrome (TS) is a neurodevelopmental disorder with a complex genetic etiology. Through an international collaboration, we genotyped 42 single nucleotide polymorphisms (p < 10(-3) ) from the recent TS genomewide association study (GWAS) in 609 independent cases and 610 ancestry-matched controls. Only rs2060546 on chromosome 12q22 (p = 3.3 × 10(-4) ) remained significant after Bonferroni correction. Meta-analysis with the original GWAS yielded the strongest association to date (p = 5.8 × 10(-7) ). Although its functional significance is unclear, rs2060546 lies closest to NTN4, an axon guidance molecule expressed in developing striatum. Risk score analysis significantly predicted case-control status (p = 0.042), suggesting that many of these variants are true TS risk alleles.