The Heritability Of And Genetic Contributions To, Frontal Electroencephalography

Abstract

The heritability of frontal EEG asymmetry, a potential endophenotype for depression, was investigated using a large set of adolescent and young adult twins. Additionally, the relationship between polymorphisms within three serotonin genes, two receptor genes and one transporter gene, and frontal EEG asymmetry was also investigated. Using Falconer's estimate, frontal EEG asymmetry was shown to be more heritable at lateral compared to medial cites across nearly all reference montages, and greater in males compared to females. Using structural equation modeling (SEM), and investigating both additive (ACE) and non-additive (ADE) models of genetic heritability, males displayed consistently greater additive genetic contributions to heritability, with greater lateral contributions than medial ones. For female twins pairs, the additive genetic model data provided a mixed picture, with more consistent heritability estimates observed at medial sites, but with larger estimates shown at lateral channels. For non-additive genetic models, male twin pairs demonstrated exclusive non-additive contributions to heritability across channels within AVG and CZ referenced data, with metrics in the CSD and LM montages more mixed between additive and non-additive contributions. However, consistent with Falconer's estimates, lateral channels were nearly always estimated to be more heritable than medial channels regardless of gender. These models demonstrate some combination of additive and non-additive contributions to the heritability of frontal EEG asymmetry, with the CSD and AVG montages showing greater lateral compared to medial heritability and CZ and LM montages showing mixed contributions with additive heritability at lateral channels and non-additive primarily at medial channels. The complex interaction of gender and reference montage on the heritability estimates highlight the subtle yet important roles of age, gender, and recording methodology when investigating proposed endophenotypes. However, no association was found between the proposed polymorphisms in serotonin receptor 1a, 2a or serotonin transporter genes and frontal EEG asymmetry. Although the results support modest heritability of frontal EEG asymmetry, the proposed link to underlying serotonergic genetic markers remains an open question. Overall, these results indicate that frontal asymmetry may be a useful endophenotype for depressive risk with modest heritability, but is one that taps more environmental risk.