The global pandemic caused by COVID-19 and the subsequent lockdown have been widely recognized as traumatic events that pose threats to psychological well-being. Recent studies reported that during such traumatic events, women tend to be at greater risk than men for developing symptoms of stress, anxiety, and depression. Several studies reported that a mindfulness-based stress reduction protocol (MBSR) provides useful skills for dealing with traumatic events. In our study, a sample of Italian females received an 8-week MBSR course plus 6 weeks of video support for meditation practice during the first total lockdown in Italy. We assessed the participants with questionnaires before and after this period to investigate their mindfulness skills, psychological well-being, post-traumatic growth, and psychological flexibility. After the intervention, the meditators group reported improvement in measures associated with self-acceptance, purpose in life, and relation to others compared to the control group. Furthermore, our results showed that participants with greater mindfulness scores showed high levels of psychological flexibility, which in turn was positively associated with higher levels of psychological well-being. We concluded that the MBSR could support psychological well-being, at least in female subjects, even during an unpredictable adverse event, such as the COVID-19 lockdown, by reinforcing key psychological aspects.

In this brief review, we present evidence of the primary role of learning-associated plasticity in the development of either adaptive or maladaptive coping strategies. Successful interactions with novel stressors foster plasticity within the neural circuits supporting acquisition, consolidation, retrieval, and extinction of instrumental learning leading to development of a rich repertoire of flexible and context-specific adaptive coping responses, whereas prolonged or repeated exposure to inescapable/uncontrollable stressors fosters dysfunctional plasticity within the learning circuits leading to perseverant and inflexible maladaptive coping strategies. Finally, the results collected using an animal model of genotype-specific coping styles indicate the engagement of different molecular networks and the opposite direction of stress effects (reduced vs. enhanced gene expression) in stressed animals, as well as different behavioral alterations, in line with differences in the symptoms profile associated with post-traumatic stress disorder.

The genetic polymorphisms involved in the physiopathology of binge eating disorder (BED) are currently unclear. This systematic review aims to highlight and summarize the research on polymorphisms that is conducted in the BED. We looked for observational studies where there was a genetic comparison between adults with BED, in some cases also with obesity or overweight, and healthy controls or obesity/overweight without BED. Our protocol was written using PRISMA. It is registered at PROSPERO (identification: CRD42020198645). To identify potentially relevant documents, the following bibliographic databases were searched without a time limit, but until September 2020: PubMed, PsycINFO, Scopus, and Web of Science. In total, 21 articles were included in the qualitative analysis of the systematic review, as they met the eligibility criteria. Within the selected studies, 41 polymorphisms of 17 genes were assessed. Overall, this systematic review provides a list of potentially useful genetic polymorphisms involved in BED: 5-HTTLPR (5-HTT), Taq1A (ANKK1/DRD2), A118G (OPRM1), C957T (DRD2), rs2283265 (DRD2), Val158Met (COMT), rs6198 (GR), Val103Ile (MC4R), Ile251Leu (MC4R), rs6265 (BNDF), and Leu72Met (GHRL). It is important to emphasize that Taq1A is the polymorphism that showed, in two different research groups, the most significant association with BED. The remaining polymorphisms need further evidence to be confirmed.

Objective: Phenylketonuria (PKU) is an inherited metabolic disease characterized by plasma hyperphenylalaninemia and several neurological symptoms that can be controlled by rigorous dietetic treatment. The cellular mechanisms underlying impaired brain functions are still unclear. It has been proposed, however, that phenylalanine interference in cognitive functions depends on impaired dopamine (DA) transmission in the prefrontal cortical area due to reduced availability of the precursor tyrosine. Here, using Pah^enu2 (ENU2) mice, the genetic murine model of PKU, we investigated all metabolic steps of catecholamine neurotransmission within the medial preFrontal Cortex (mpFC), availability of the precursor tyrosine, synthesis and release, to find an easy way to reinstate normal cortical DA neurotransmission.Methods and results: Analysis of blood and brain levels of tyrosine showed reduced plasma and cerebral levels of tyrosine in ENU2 mice. Western blot analysis demonstrated deficient tyrosine hydroxylase (TH) protein levels in mpFC of ENU2 mice. Cortical TH activity, determined in vivo by measuring the accumulation of l‐3,4‐dihydroxyphenylalanine (L‐DOPA) in mpFC after inhibition of L‐aromatic acid decarboxylase with NSD‐1015, was reduced in ENU2 mice. Finally, a very low dose of L‐DOPA, which bypasses the phenylalanine‐inhibited metabolic steps, restored DA prefrontal transmission to levels found in healthy mice.Conclusion: The data suggests that a strategy of using tyrosine supplementation to treat PKU is unlikely to be effective, whereas small dose L‐DOPA administration is likely to have a positive therapeutic effect.