A missense variant (P10L) of the melanopsin (OPN4) gene in seasonal affective disorder

Sep 23, 2008Journal of affective disorders

A genetic change in the light-sensitive melanopsin gene linked to seasonal depression

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Abstract

SAD participants had a 5.6 times higher likelihood of carrying the T/T genotype for the melanopsin variant rs2675703 compared to controls.

Individuals with the homozygous minor genotype (T/T) for the missense variant rs2675703 were exclusively found in the SAD group.
The frequency of the T/T genotype was significantly higher in SAD participants than in controls, who had C/C and C/T genotypes.
These findings suggest a potential genetic predisposition linked to abnormal light responses in Seasonal Affective Disorder.
The study focused on one specific genetic variant related to the non-visual light input pathway.

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BACKGROUND: Melanopsin, a non-visual photopigment, may play a role in aberrant responses to low winter light levels in Seasonal Affective Disorder (SAD). We hypothesize that functional sequence variation in the melanopsin gene could contribute to increasing the light needed for normal functioning during winter in SAD.

METHODS: Associations between alleles, genotypes, and haplotypes of melanopsin in SAD participants (n=130) were performed relative to controls with no history of psychopathology (n=90).

RESULTS: SAD participants had a higher frequency of the homozygous minor genotype (T/T) for the missense variant rs2675703 (P10L) than controls, compared to the combined frequencies of C/C and C/T. Individuals with the T/T genotype were 5.6 times more likely to be in the SAD group than the control group, and all 7 (5%) of individuals with the T/T genotype at P10L were in the SAD group.

LIMITATIONS: The study examined only one molecular component of the non-visual light input pathway, and recruitment methods for the comparison groups differed.

CONCLUSION: These findings support the hypothesis that melanopsin variants may predispose some individuals to SAD. Characterizing the genetic basis for deficits in the non-visual light input pathway has the potential to define mechanisms underlying the pathological response to light in SAD, which may improve treatment.

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A missense variant (P10L) of the melanopsin (OPN4) gene in seasonal affective disorder

Abstract

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