Disturbances of serotonergic neurotransmission and temperamental vulnerability have both been implicated in the pathogenesis of anorexia nervosa (AN). We genotyped the –1438 A/G polymorphism in the 5-HT2A receptor gene and serotonin transporter linked-polymorphic region (5-HTTLPR) in 132 adolescent subjects with AN and in 93 healthy controls. Personality dimensions in AN patients were assessed with the Temperament and Character Inventory. In a case-control model, we tested the hypothesis that these genetic variants confer susceptibility to AN. We also analyzed whether two polymorphisms show association with temperamental and character traits. No significant difference was found in the 5-HTTLPR frequency between AN patients and controls; however, there was a statistical trend towards a higher frequency of the A allele of the –1438 A/G polymorphism in patients than in controls (64.9 vs. 56.7%, χ2 test, p = 0.08). We also found a significant association between the A allele of this polymorphism and two temperamental traits. Patients homozygous for the A allele showed lower reward dependence than G/G homozygotes, and A/A homozygotes showed lower harm avoidance than heterozygotes. Low reward dependence and harm avoidance were more characteristic of the restrictive-type AN than of other subtypes of the disorder. No association of 5-HTTLPR with personality dimensions in AN patients was observed. Our results may suggest that the A allele of the –1438 A/G polymorphism confers some genetic risk for adolescent AN patients, especially in those with personality traits, which are typical of the restrictive-type AN.

Patients with anorexia nervosa (AN) experience difficulties in neurocognitive functioning in the acute phase of illness which might be related to clinical presentation, but also in the apparently remitted state after weight recovery. Among the most commonly reported persistent deficits is cognitive inflexibility, which can be interpreted as a vulnerability trait or a “neuropsychological scar” reflecting the detrimental effect of prolonged semi-starvation in patients with a long duration of illness. Studies of adolescent samples with a relatively short clinical course may enable avoiding the effect of prolonged illness and help to determine whether neuropsychological deficits are trait or state dependent. The aim of this study is to assess cognitive functioning in adolescents with AN before and after the inpatient treatment programme, including cognitive remediation therapy (CRT). Forty-seven adolescent female inpatients with AN diagnosed according to DSM-5 and fifty healthy female adolescents matched for the education level and age were recruited. The patients underwent a multimodal treatment including a ten-week CRT. The standardized and cross-validated neuropsychological (Trail Making Test – TMT A and B, Color-Word Stroop Task – CWST, Ruff Figural Fluency Test – RFFT) and clinical measurements (Beck Depression Inventory – BDI, Eating Attitude Test – EAT-26, Yale-Brown Obsessive Compulsive Scale – Y-BOCS) were used to assess both clinical (in the acute phase and after partial weight recovery) and control subjects. Initially, AN patients performed significantly worse compared to the controls, but afterwards, inpatient treatment improvement was noted on all examined measures. In a few subtests (TMT, CWST) performance of AN patients after the programme was still significantly poorer than in HC. Cognitive inflexibility in adolescent AN patients, as measured with TMT, CWST, and RFFT tends to improve after therapy. Nevertheless, a few neuropsychological subtests which did not show complete normalization may warrant attention in subsequent studies. Further research including control intervention is needed to conclude whether CRT intervention affects the outcome.

Introduction: Depression is the most prevalent comorbid neuropsychiatric condition in individuals with Parkinson’s disease (PD), and its underlying mechanisms are not yet fully understood. Current treatment methods are characterised by moderate effectiveness and possible side effects, prompting the search for new non-invasive and safe treatment methods. Methods: This narrative review explores the use of transcranial direct current stimulation (tDCS) in the treatment of depression in PD, based on neuropsychological measures. Searches were conducted in the PubMed/Medline, Research Gate, and Cochrane databases. Results: Nine relevant studies were identified, where depression scores served as either primary or secondary outcomes. Stimulation protocols displayed heterogeneity, especially concerning choice of stimulation site. Patient samples were also heterogeneous. The majority of the studies incorporated anodal stimulation targeting the left dorsolateral prefrontal cortex (DLPFC). The results revealed a reduction in depression scores among PD patients following tDCS. Potential mechanisms through which tDCS may alleviate depression in PD were discussed and recommendations for future research were made. Conclusions: Preliminary evidence suggests that tDCS applied anodally to the left DLPFC reduces depression scores in people with PD; however, due to the heterogeneity of the studies analysed, the use of tDCS in this field should be approached with caution and warrants further validation and confirmation.

Eating disorders—including anorexia nervosa (AN), bulimia nervosa, and binge eating disorder—are clinically distinct but exhibit symptom overlap and diagnostic crossover. Genomic analyses have mostly examined AN. We conducted the first genomic meta-analysis of binge-eating behaviour (BE; 39,279 cases, 1,227,436 controls), alongside new analyses of AN (24,223 cases, 1,243,971 controls) and its subtypes (all European ancestries). We identified six loci associated with BE, including loci associated with higher body mass index (BMI) and impulse-control behaviours. AN GWAS yielded eight loci, validating six loci. Subsequent polygenic risk score analysis demonstrated an association with AN in two East Asian ancestry cohorts. BE and AN exhibited similar positive genetic correlations with psychiatric disorders, but opposing genetic correlations with anthropometric traits. Most of the genetic signal in BE and AN was not shared with BMI. We have extended eating disorder genomics beyond AN; future work will incorporate multiple diagnoses and global ancestries.