ArticleFrontiers in aging neuroscience2010
COMT Val158Met Polymorphism Modulates Cognitive Effects of Dietary Intervention.
Article in Frontiers in aging neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Association of Cognition-Related Genetic Polymorphisms with Elite Athlete Status: A Meta-Analysis.Genes · 2026Pooled it
- Genetic Variation in Response to the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND): A Randomized Controlled Trial.Nutrients · 2026Trial
- Primary Metabolites in ThreeLife (Basel, Switzerland) · 2026Article
- Aging and a genetic KIBRA polymorphism interactively affect feedback- and observation-based probabilistic classification learning.Neurobiology of aging · 2018Article
- COMT Val158Met polymorphism is associated with blood pressure and lipid levels in general families of Bama longevous area in China.International journal of clinical and experimental pathology · 2015Article
- The association between the catechol-O-methyltransferase Val108/158Met polymorphism and hyperactive-impulsive and inattentive symptoms in youth.Psychopharmacology · 2013Article
- Interaction of BDNF and COMT polymorphisms on paired-associative stimulation-induced cortical plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- [Lifestyle and cognition: what do we know from the aging and neurodegenerative brain?].Der Nervenarzt · 2011Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A common single nucleotide polymorphism (SNP) in the gene encoding catechol-O-methyltransferase (COMT), Val158Met, is thought to influence cognitive performance due to differences in prefrontal dopaminergic neurotransmission. Previous studies lend support for the hypothesis that the "at risk" genotype comprising two Val-alleles (low dopamine) might benefit more from plasticity-enhancing interventions than carriers of one or two Met-alleles. This study aimed to determine whether the response to dietary interventions, known to modulate cognition, is dependent on COMT genotype. Blood samples of 35 healthy elderly subjects (61.3 years ±8 SD; 19 women, 16 men, BMI: 28.2 kg/m(2) ±4 SD) were genotyped for COMT Val158Met by standard procedures (Val/Val = 6; Val/Met = 20; Met/Met = 9). Subjects had previously completed a randomized controlled trial investigating the effects of caloric restriction (CR) or enhancement of unsaturated fatty acids (UFA) on immediate and delayed verbal recognition memory. Homozygous Val/Val-carriers had significantly lower memory scores than Met-carriers at baseline (p < 0.001). Significant interactions of genotype and dietary intervention with regard to cognition were found: CR- and UFA enhancement-induced memory improvements of Val/Val-carriers were considerably greater than those of Met-carriers (ANOVA p's < 0.02). The current study shows for the first time that cognitive effects of dietary interventions are dependent on COMT Val158Met genotype. Our findings lend further support to the hypothesis that an "at risk" genotype might benefit more from plasticity-enhancing interventions than the "not at risk" genotype. This might help to develop individualized therapies in future research based on genetic background.
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