Background: International research has emphasized that youths are at higher risk for the onset of internet addiction (IA), but studies investigating biological, psychological, and social factors associated with this condition are limited. Objective: This study aims to investigate the possible association between IA and genetic polymorphisms in monoamine oxidase A (MAO-A), serotonin-transporter (5-HTTPR), dopamine receptor (DRD4), and dopamine transporter (DAT1) genes by considering the role played by the perception of young adults in their family functioning and their depression, anxiety, and avoidant personality problems. Methods: In a sample of 104 male and female young adults aged between 19 and 23 years (mean age 21.87, SD 2.29 years) recruited from universities in the central southern part of Italy, we addressed the presence of IA using the Young criteria of the IA test. Moreover, the perception of young adults of their family functioning and their psychopathological symptoms were assessed through the Family Assessment Device (FAD) and the Adult Self-Report, respectively. Results: We found no significant association between IA and any genetic polymorphisms, neither among males or females. Young adults with IA reported significantly higher scores in the subscale of FAD affective responsiveness (AR; P=.01) and in depressive problems (P=.02), anxiety problems (P=.009), and avoidant personality problems (P=.003) than those in the control group. Results of mediation analyses showed a mediation role played by depressive symptoms (B=0.99; 95% CI 0.22 to 1.97) and avoidant personality problems (B=1.09; 95% CI 0.32 to 2.05) of young adults on the relationship between the FAD, AR, and IA. Finally, this relationship was moderated by the genotype of the 5-HTTLPR (P<.001), DAT1 (P<.001), and MAO-A (P<.001) genes in young adults. Conclusions: This exploratory study supports the recent evidence on the mutual relationship among biological, individual, and social risk factors associated with IA in young adulthood. Our findings may have important clinical implications for the development of prevention and treatment programs.

Parental psychopathological risk is considered as one of the most crucial features associated with epigenetic modifications in offspring, which in turn are thought to be related to their emotional/behavioral profiles. The dopamine active transporter (DAT) gene is suggested to play a significant role in affective/behavioral regulation. On the basis of the previous literature, we aimed at verifying whether children’s DAT1 polymorphisms moderated the relationship between parents’ psychological profiles, children’s emotional/behavioral functioning, and DAT1 methylation in a normative sample of 79 families with school-age children (Ntot = 237). Children’s biological samples were collected through buccal swabs, while Symptom Check-List-90 item Revised, Adult Self Report, and Child Behavior Check-List/6–18 was administered to assess parental and children’s psychological functioning. We found that higher maternal externalizing problems predicted the following: higher levels of children’s DAT1 methylation at M1, but only among children with 10/10 genotype; higher levels of methylation at M2 among children with 10/10 genotype; while lower levels for children with a 9-repeat allele. There was also a positive relationship between fathers’ externalizing problems and children’s externalizing problems, only for children with a 9-repeat allele. Our findings support emerging evidence of the complex interplay between genetic and environmental factors in shaping children’ emotional/behavioral functioning, contributing to the knowledge of risk variables for a child’s development and psychological well-being.

The microtubule-associated protein tau (MAPT) region has been conceptualized as a model of the interaction between genetics and functional disease outcomes in neurodegenerative disorders, such as Parkinson disease. Indeed, haplotype-specific differences in expression and alternative splicing of MAPT transcripts affect cellular functions at different levels, increasing susceptibility to a range of neurodegenerative processes. In order to evaluate a possible link between MAPT variants, PD risk and PD motor phenotype, we analyzed the genetic architecture of MAPT in a cohort of PD patients. We observed a statistically significant association between the H1 haplotype and PD risk (79.5 vs 69.5%; 2 =9.9; OR,1.7; 95% CI, 1.2-2.4; p=0.002). The effect was more evident in non tremor dominant PD subjects (NTD-PD) (82 vs 69.5%; 2 =13.6; OR, 2.03; 95% CI, 1.4-3; p=0.0003), while no difference emerged between PD subgroup of tremor dominant patients (TD-PD) and control subjects. Examination of specific intra-H1 variations showed that the H1h subhaplotype was overrepresented in NTD-PD patients compared with controls (p=0.007, OR 2.9; 95%CI 1.3-6.3). Although we cannot exclude that MAPT variation may be associated with ethnicity, our results may support the hypothesis that MAPT H1 clade and a specific H1 subhaplotype influence the risk of PD and modulate the clinical expression of the disease, including motor phenotype.

Internet influences our communication, social and work interactions, entertainment, and many other aspects of life. Even if the original purpose was to simplify our lives, an excessive and/or maladaptive use of it may have negative consequences. The dopamine transporter (DAT1) gene was studied in relation to addictions, including excessive use of the Internet. The crucial role of DAT1 was previously underlined in modulating emotional aspects, such as affiliative behaviors. The present research follows a new approach based on cross-correlation between (de)methylation levels in couples of CpG loci, as previously shown. We investigated the possible relationships between Internet addiction, impulsivity, quality of attachment, DAT1 genotypes (from the 3′-untranslated region (UTR) variable number of tandem repeats (VNTR) poly-morphism), and the dynamics of methylation within the 5’-UTR of the DAT1 gene. From a normative sample of 79 youths, we extrapolated three subgroups a posteriori, i.e., one “vulnerable” with high Internet Addiction Test (IAT) scores (and high Barrat Impulsivity Scale (BIS) scores; n = 9) and two “controls’’ with low BIS scores and 10/10 vs. 9/x genotype (n = 12 each). Controls also had a “secure” attachment pattern, while genotypes and attachment styles were undistinguished in the vulnerable subgroup (none showed overt Internet addiction). We found a strongly positive correlation in all groups between CpG2 and CpG3. An unsuspected relationship between the 3’-UTR genotype and a 5’-UTR intra-motif link was revealed by CpG5–CpG6 comparison. The negative correlation between the CpG3–CpG5 positions was quite significant in the control groups (both with genotype 10/10 and with genotype 9/x), whereas a tendency toward positive correlation emerged within the high IAT group. In conclusion, future attention shall be focused on the intra- and inter-motif interactions of methylation on the CpG island at the 5′-UTR of DAT1.