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Mark A. Sabbagh - One of the best experts on this subject based on the ideXlab platform.

  • Mental state decoding in past major Depression: Effect of sad versus happy mood induction
    Cognition & Emotion, 2010
    Co-Authors: Kate L. Harkness, Jill A. Jacobson, David Duong, Mark A. Sabbagh
    Abstract:

    Individuals with mild Depression show an enhanced ability to read or “decode” others' mental states. The goal of the present study was to investigate whether this pattern of performance is related specifically to the Pathology of Depression or whether it is simply a feature of the transient dysphoric state. Forty-one undergraduates with a previous episode of major Depression and 52 undergraduates with no Depression history participated in a mental state decoding task following a sad versus happy mood induction. Previously depressed participants were significantly more accurate in their mental state judgements than were the never-depressed participants, suggesting that enhanced mental state decoding may be a specific feature of Depression in remission. Furthermore, previously depressed participants whose positive mood increased in response to the happy mood induction showed a poorer level of performance on the task, similar to that observed in the never-depressed group. Thus, a happy mood may have induced ...

Bernhard T Baune - One of the best experts on this subject based on the ideXlab platform.

  • possible associations of ntrk2 polymorphisms with antidepressant treatment outcome findings from an extended tag snp approach
    PLOS ONE, 2013
    Co-Authors: J Hennings, Martin A Kohli, Darina Czamara, Maria Giese, Anne Eckert, Christiane Wolf, Angela Heck, Katharina Domschke, Volker Arolt, Bernhard T Baune
    Abstract:

    Background: Data from clinical studies and results from animal models suggest an involvement of the neurotrophin system in the Pathology of Depression and antidepressant treatment response. Genetic variations within the genes coding for the brain-derived neurotrophic factor (BDNF) and its key receptor Trkb (NTRK2) may therefore influence the response to antidepressant treatment. Methods: We performed a single and multi-marker association study with antidepressant treatment outcome in 398 depressed Caucasian inpatients participating in the Munich Antidepressant Response Signature (MARS) project. Two Caucasian replication samples (N=249 and N=247) were investigated, resulting in a total number of 894 patients. 18 tagging SNPs in the BDNF gene region and 64 tagging SNPs in the NTRK2 gene region were genotyped in the discovery sample; 16 nominally associated SNPs were tested in two replication samples. Results: In the discovery analysis, 7 BDNF SNPs and 9 NTRK2 SNPs were nominally associated with treatment response. Three NTRK2 SNPs (rs10868223, rs1659412 and rs11140778) also showed associations in at least one replication sample and in the combined sample with the same direction of effects (Pcorr=.018, Pcorr=.015 and Pcorr=.004, respectively). We observed an across-gene BDNF-NTRK2 SNP interaction for rs4923468 and rs1387926. No robust interaction of associated SNPs was found in an analysis of BDNF serum protein levels as a predictor for treatment outcome in a subset of 93 patients. Conclusions/Limitations: Although not all associations in the discovery analysis could be unambiguously replicated, the findings of the present study identified single nucleotide variations in the BDNF and NTRK2 genes that might be involved in antidepressant treatment outcome and that have not been previously reported in this context. These new variants need further validation in future association studies.

Huiling Wang - One of the best experts on this subject based on the ideXlab platform.

  • dihydrolipoic acid protects against lipopolysaccharide induced behavioral deficits and neuroinflammation via regulation of nrf2 ho 1 nlrp3 signaling in rat
    Journal of Neuroinflammation, 2020
    Co-Authors: Hetao Bian, Gaohua Wang, Junjie Huang, Liang Liang, Yage Zheng, Yanyan Wei, Hui Wang, Ling Xiao, Huiling Wang
    Abstract:

    Recently, Depression has been identified as a prevalent and severe mental disorder. However, the mechanisms underlying the Depression risk remain elusive. The neuroinflammation and NLRP3 inflammasome activation are known to be involved in the Pathology of Depression. Dihydrolipoic acid (DHLA) has been reported as a strong antioxidant and exhibits anti-inflammatory properties in various diseases, albeit the direct relevance between DHLA and Depression is yet unknown. The present study aimed to investigate the preventive effect and potential mechanism of DHLA in the lipopolysaccharide (LPS)-induced sickness behavior in rats. Adult male Sprague–Dawley rats were utilized. LPS and DHLA were injected intraperitoneally every 2 days and daily, respectively. Fluoxetine (Flu) was injected intraperitoneally daily. PD98059, an inhibitor of ERK, was injected intraperitoneally 1 h before DHLA injection daily. Small interfering ribonucleic acid (siRNA) for nuclear factor erythroid 2-like (Nrf2) was injected into the bilateral hippocampus 14 days before the DHLA injection. Depression-like behavior tests were performed. Western blot and immunofluorescence staining detected the ERK/Nrf2/HO-1/ROS/NLRP3 pathway-related proteins. The DHLA and fluoxetine treatment exerted preventive effects in LPS-induced sickness behavior rats. The DHLA treatment increased the expression of ERK, Nrf2, and HO-1 but decreased the ROS generation levels and reduced the expression of NLRP3, caspase-1, and IL-1β in LPS-induced sickness behavior rats. PD98059 abolished the effects of DHLA on preventive effect as well as the levels of Nrf2 and HO-1 proteins. Similarly, Nrf2 siRNA reversed the preventive effect of DHLA administration via the decreased expression of HO-1. These findings suggested that DHLA exerted a preventive effect via ERK/Nrf2/HO-1/ROS/NLRP3 pathway in LPS-induced sickness behavior rats. Thus, DHLA may serve as a potential therapeutic strategy for Depression.

Weiku Zhang - One of the best experts on this subject based on the ideXlab platform.

  • identifying the mechanism underlying antidepressant like effects of loganin by network pharmacology in combination with experimental validation
    Journal of Ethnopharmacology, 2021
    Co-Authors: Cong-yuan Xia, Yu Yan, Wen-wen Lian, Weiku Zhang
    Abstract:

    Abstract Ethnopharmacological relevance Loganin, an iridoid glycoside, is one of the quality control indexes of Cornus officinalis Sieb. et Zucc. Increasing evidence emphasize the important role of inflammation in the Pathology of Depression, which links Depression with other chronic diseases. Loganin prevents inflammatory response in multiple diseases and reverses depressive-like behaviors. However, the mechanisms underlying antidepressant-like effects of loganin for the treatment of inflammation-associated Depression are not utterly understood. Aim of the study The present study was designed to predict the potential targets of loganin against inflammation-associated Depression using a network pharmacology approach. Materials and methods Pharmmapper and Uniport were used to predict loganin-related targets. Targets of inflammation were identified through GeneCards databases and Online Mendelian Inheritance in Man (OMIM). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were used to identify the potential mechanism. Finally, qRT-PCR and ELISA were used to confirm the role of loganin on these targets. Results There were 15 nodes in the loganin-inflammation-Depression intersection targets network. In the network, the degree value of CTNNB1 was above 3. Among top ten pathways identified by KEGG analysis, Th1/Th2 cell differentiation and IL-17 signaling pathways were related with both inflammation and Depression. As indicated by qRT-PCR results, loganin increased CTNNB1 mRNA level. Moreover, loganin elevated M2 markers of microglia but decreased M1 markers of microglia against lipopolysaccharide (LPS), indicated by qRT-PCR results and ELISA results. Conclusion CTNNB1 was the main target of loganin. Loganin alleviated LPS-induced inflammation through inhibiting M1 polarization of microglia. Our results provide a better understanding of loganin-induced antidepressant-like effects for the treatment of inflammation-associated Depression.

Thomas Frodl - One of the best experts on this subject based on the ideXlab platform.

  • Meta-analysis of diffusion tensor imaging studies shows altered fractional anisotropy occurring in distinct brain areas in association with Depression
    Biology of mood & anxiety disorders, 2011
    Co-Authors: Melissa L. Murphy, Thomas Frodl
    Abstract:

    Fractional anisotropy anomalies occurring in the white matter tracts in the brains of depressed patients may reflect microstructural changes underlying the pathophysiology of this disorder. We conducted a meta-analysis of fractional anisotropy abnormalities occurring in major depressive disorder using voxel-based diffusion tensor imaging studies. Using the Embase, PubMed and Google Scholar databases, 89 relevant data sets were identified, of which 7 (including 188 patients with major depressive disorder and 221 healthy controls) met our inclusion criteria. Authors were contacted to retrieve any additional data required. Coordinates were extracted from clusters of significant white matter fractional anisotropy differences between patients and controls. Relevant demographic, clinical and methodological variables were extracted from each study or obtained directly from authors. The meta-analysis was carried out using Signed Differential Mapping. Patients with Depression showed decreased white matter fractional anisotropy values in the superior longitudinal fasciculus and increased fractional anisotropy values in the fronto-occipital fasciculus compared to controls. Using quartile and jackknife sensitivity analysis, we found that reduced fractional anisotropy in the left superior longitudinal fasciculus was very stable, with increases in the right fronto-occipital fasciculus driven by just one study. In conclusion, our meta-analysis revealed a significant reduction in fractional anisotropy values in the left superior longitudinal fasciculus, which may ultimately play an important role in the Pathology of Depression.