Mental health literacy about depression and schizophrenia among adolescents in Sweden.

BACKGROUND: Mental health literacy (MHL) refers to an individual's knowledge of mental disorders, including the ability to recognize psychopathology and being aware of help options. Most studies of MHL have focused on adults. OBJECTIVE: The purpose of this study was to examine levels of MHL among adolescents. METHODS: MHL was examined using two pre-established vignettes that presented an adolescent with symptoms of either depression or schizophrenia. The respondents were 426 adolescents (age mean=16). Vignette data were analyzed both qualitatively and quantitatively. RESULTS: The data showed that 42.7% and 34.7% of the respondents identified depression and schizophrenia, respectively. Depression was recognized more often by females than males. Professional help was suggested by a minority of the respondents for managing symptoms of depression (22.5%) or schizophrenia (32.6%). Altruistic behaviors, examined through the willingness to help an acquaintance with mental illness symptoms, were apparent among 58.2% of the respondents and to a greater extent in females than males. Answers following the schizophrenia vignette also revealed stigmatizing attitudes in 11.5% of the participants. CONCLUSIONS: There are relatively low levels of MHL among teenagers in Sweden. Awareness campaigns and the implementation of psychoeducation in the school curriculum could increase MHL in this group.

Allele-specific programming of Npy and epigenetic effects of physical activity in a genetic model of depression.

Neuropeptide Y (NPY) has been implicated in depression, emotional processing and stress response. Part of this evidence originates from human single-nucleotide polymorphism (SNP) studies. In the present study, we report that a SNP in the rat Npy promoter (C/T; rs105431668) affects in vitro transcription and DNA-protein interactions. Genotyping studies showed that the C-allele of rs105431668 is present in a genetic rat model of depression (Flinders sensitive line; FSL), while the SNP's T-allele is present in its controls (Flinders resistant line; FRL). In vivo experiments revealed binding of a transcription factor (CREB2) and a histone acetyltransferase (Ep300) only at the SNP locus of the FRL. Accordingly, the FRL had increased hippocampal levels of Npy mRNA and H3K18 acetylation; a gene-activating histone modification maintained by Ep300. Next, based on previous studies showing antidepressant-like effects of physical activity in the FSL, we hypothesized that physical activity may affect Npy's epigenetic status. In line with this assumption, physical activity was associated with increased levels of Npy mRNA and H3K18 acetylation. Physical activity was also associated with reduced mRNA levels of a histone deacetylase (Hdac5). Conclusively, the rat rs105431668 appears to be a functional Npy SNP that may underlie depression-like characteristics. In addition, the achieved epigenetic reprogramming of Npy provides molecular support for the putative effectiveness of physical activity as a non-pharmacological antidepressant.

Long-term lithium treatment in bipolar disorder is associated with longer leukocyte telomeres.

Telomere shortening is a hallmark of aging and has been associated with oxidative stress, inflammation and chronic somatic, as well as psychiatric disorders, including schizophrenia and depression. Additionally, antidepressants have been found to protect against telomere shortening. However, pharmacological telomere studies are lacking in bipolar disorder (BD). Therefore, the objective of this study was to explore telomere length (TL) in patients with BD in the context of lithium treatment. We determined TL by quantitative real-time PCR using peripheral blood leukocytes. Participants were outpatients diagnosed with BD type 1 or 2 (n=256) and healthy controls (n=139). Retrospective case-control and case-case study designs were applied. Lithium response (LiR) was scored using the Alda-Scale. Lithium-treated BD patients overall, as well as those on lithium monotherapy, had 35% longer telomeres compared with controls (P<0.0005, partial η(2)=0.13). TL correlated positively with lithium treatment duration of >30 months (P=0.031, R(2)=0.13) and was negatively associated with increasing number of depressive episodes (P<0.007). BD patients responding well to lithium treatment had longer telomeres than those not responding well. This is the first study to report a positive effect of long-term lithium treatment on TL. Importantly, longer TL was also associated with a better LiR in BD patients. These data suggest that lithium exerts a protective effect against telomere shortening especially when therapeutically efficacious. We hypothesize that induction of telomerase activity may be involved in LiR in BD.