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Coenzyme Q 10  (CoQ 10 ) is a lipophilic redox molecule that is present in membranes of almost all cells in human tissues. CoQ 10  is, amongst other functions, essential for the respiratory transport chain and is a modulator of inflammatory processes and gene expression. Rare monogenetic CoQ 10  deficiencies show noticeable symptoms in tissues (e.g. kidney) and cell types (e.g. neurons) with a high energy demand. To identify common genetic variants influencing serum CoQ 10  levels, we performed a fixed effects meta-analysis in two independent cross-sectional Northern German cohorts comprising 1300 individuals in total. We identified two genome-wide significant susceptibility loci. The best associated single nucleotide polymorphism (SNP) was rs9952641 ( P  value = 1.31 × 10  −   8 , β = 0.063, CI 0.95  [0.041, 0.085]) within the  COLEC12  gene on chromosome 18. The SNP rs933585 within the  NRXN-1  gene on chromosome 2 also showed genome wide significance ( P  value = 3.64 × 10  −   8 , β = −0.034, CI 0.95  [−0.046, −0.022]). Both genes have been previously linked to neuronal diseases like Alzheimer's disease, autism and schizophrenia. Among our ‘top-10’ associated variants, four additional loci with known neuronal connections showed suggestive associations with CoQ 10  levels. In summary, this study demonstrates that serum CoQ 10  levels are associated with common genetic loci that are linked to neuronal diseases.

Genome-wide association study of serum coenzyme Q 10 levels identifies susceptibility loci linked to neuronal diseases