Genetic factors linked to aberrant neural activity of individuals with substance use disorder phenotypes: A systematic review and meta-analysis of EEG studies

Abstract

Background: Alterations in EEG activity have been considered valid endophenotypes of substance use disorders (SUDs). Empirical evidence has supported the association between genetic factors (e.g., genes, single nucleotide polymorphisms [SNPs]) and SUDs, considering both clinical samples and individuals with a positive family history of SUDs [F⁺SUD]). Nevertheless, the relationship between genetic factors and intermediate phenotypes (i.e., altered EEG activity) among individuals with SUD phenotypes remains unclear.

Objective(s): The current study aims at summarizing genetic factors linked to aberrant EEG activity among individuals with SUDs and those with F⁺SUD.

Methods: Sixteen studies (5 [N = 986] + 11 from the Collaborative Studies On Genetics of Alcoholism [COGA] sample [432 ≤ N ≤ 8810]) were included for a qualitative systematic review. Thirteen studies (5 + 8 studies from the COGA sample) were used for multi-level meta-analytic procedures.

Results: Qualitative analyses highlighted a multivariate genetic architecture linked to alterations in EEG waves among individuals with SUD phenotypes (i.e., augmented resting-state beta waves; reduced resting-state alpha waves; reduced resting-state and task-dependent theta waves). The most recurrent genetic factors were involved in cellular energy homeostasis, modulation of inhibitory and excitatory neural activity together with neural cell growth. Meta-analytic results showed a moderate association between genetic factors and altered resting-state and task-dependent EEG activity. Meta-analytic results also suggested non-additive genetic effects on altered EEG activity.

Conclusions: Complex genetic interactions mediating neural activity and brain development might constitute a causal pathway toward intermediate phenotypes associated with phenotypic features, which in turn are linked to SUDs.

Keywords:

• Substance use disorders
• EEG activity
• genetic factors
• non-additive effects
• development

Disclosure statement

The authors report no relevant financial conflicts. This work did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sector. The authors alone are responsible for the content and writing of this paper.

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Funding

The author(s) reported there is no funding associated with the work featured in this article.