Progress in Neuro-Psychopharmacology & Biological Psychiatry最新文献

{"title":"Understanding sex and populational differences in spatio-temporal exploration patterns and homebase dynamics of zebrafish following repeated ethanol exposure","authors":"Cássio M. Resmim ,&nbsp;João V. Borba ,&nbsp;Falco L. Gonçalves ,&nbsp;Laura W. Santos ,&nbsp;Julia Canzian ,&nbsp;Barbara D. Fontana ,&nbsp;Maribel A. Rubin ,&nbsp;Denis B. Rosemberg","doi":"10.1016/j.pnpbp.2024.111171","DOIUrl":"10.1016/j.pnpbp.2024.111171","url":null,"abstract":"<div><div>Ethanol (EtOH) is one of the most widely consumed substance, affecting neurobehavioral functions depending on multiple environmental and biological factors. Although EtOH modulates zebrafish (<em>Danio rerio</em>) anxiety-like behaviors in novelty-based paradigms, the potential role of biological sex and populational variability in the exploratory dynamics in the open field test (OFT) is unknown. Here, we explored whether a repeated EtOH exposure protocol modulates the spatio-temporal exploration and homebase-related parameters in a population- and sex-dependent manner. Male and female fish from the short-fin (SF) and leopard (LEO) phenotypes were exposed to EtOH for 7 days (1 % <em>v</em>/v, 20 min per day). On the 8th day, the OFT was performed to assess locomotor and exploratory behaviors. We verified significant populational differences in the baseline spatio-temporal exploration patterns, supporting a pronounced anxiety in LEO with a higher homebase index compared to SF. We also found sex-dependent differences in EtOH sensitivity, where SF was more sensitive to EtOH, especially in females, which showed marked alterations in thigmotaxis and homebase occupancy. Conversely, only LEO female subjects showed increased center occupancy following EtOH. Principal component analysis (PCA) showed the main components that explained data variability, which were sex- and population-dependent. Overall, our novel findings support the utility of zebrafish-based models to assess how EtOH influences the exploratory profile in the OFT, as well as to elucidate potential differences of sex and population in the neurobehavioral responses of alcohol exposure in a translational perspective.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111171"},"PeriodicalIF":5.3,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142445843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between intestinal fatty-acid binding protein and clinical and metabolic characteristics of depression","authors":"Oliwia Gawlik-Kotelnicka ,&nbsp;Karolina Czarnecka-Chrebelska ,&nbsp;Aleksandra Margulska ,&nbsp;Ewa Pikus ,&nbsp;Jakub Wasiak ,&nbsp;Anna Skowrońska ,&nbsp;Ewa Brzeziańska-Lasota ,&nbsp;Dominik Strzelecki","doi":"10.1016/j.pnpbp.2024.111170","DOIUrl":"10.1016/j.pnpbp.2024.111170","url":null,"abstract":"<div><div>Introduction: The topic of increased intestinal permeability is associated with disruption of the intestinal barrier, leading to the “leaky gut” syndrome. Depressive disorders often coexist with abdominal obesity, metabolic syndrome, or its components and complications. Intestinal permeability has been proven to relate to all of the above. Methods: In this cross-sectional study, we aimed to assess the “leaky gut” blood biomarker - intestinal fatty acid-binding protein (I-FABP) - in 114 adult patients diagnosed with depressive disorders depending on abdominal obesity comorbidity, depression, anxiety, and stress level, or antidepressant use. The corrected <em>p</em>-value was set at 0.02. We analyzed patients' mental state, diet, anthropometric parameters, metabolic laboratory markers and I-FABP. Results: There was no difference in circulating I-FABP levels between obese and non-obese patients with depressive disorders (<em>p</em> = 0.648). Similarly, I-FABP levels were not different in patients with different emotional symptoms severity (<em>p</em> = 0.829 for self-assessed depression, <em>p</em> = 0.164 for anxiety, and <em>p</em> = 0.543 for stress). But, I-FABP levels differed significantly between patients treated and not treated with antidepressants (<em>p</em> = 0.011). In general linear model analysis treatment with antidepressants, anxiety severity level, their interaction, along with smoking status, drinks intake, and using dietary supplements were shown to significantly explain I-FABP variance (<em>p</em> &lt; 0.001, R²_adj = 0.261). Conclusions: Comorbid obesity did not increase intestinal permeability circulating marker, I-FABP, in the population of patients with depressive disorders. Treatment with antidepressants may be connected to higher I-FABP levels. Using dietary supplements, drinks intake, smoking status, or anxiety level may serve as explanatory factors.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111170"},"PeriodicalIF":5.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142407180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic association and drug target exploration of inflammation-related proteins with risk of major depressive disorder","authors":"Wenxi Sun ,&nbsp;Hongbao Cao ,&nbsp;Dongming Liu ,&nbsp;Ancha Baranova ,&nbsp;Fuquan Zhang ,&nbsp;Xiaobin Zhang","doi":"10.1016/j.pnpbp.2024.111165","DOIUrl":"10.1016/j.pnpbp.2024.111165","url":null,"abstract":"<div><h3>Background</h3><div>In numerous observational studies, circulating inflammation-related proteins have been linked with major depressive disorder (MDD), yet the precise causal direction of this relationship remains unclear. This study aims to investigate the potential causal link between inflammation-related proteins and the risk of developing MDD.</div></div><div><h3>Methods</h3><div>We utilized summary data from a genome-wide association study (GWAS) of 91 circulating inflammation-associated proteins in 14,824 individuals of European descent. Additionally, we incorporated findings from a substantial GWAS on MDD, which included 294,322 cases and 741,438 controls. Our analysis employed a two-sample bidirectional Mendelian randomization (MR) approach, with inverse variance weighting (IVW) as the primary method. We augmented this with two supplementary techniques (MR-Egger and weighted median approaches) to detect and address potential pleiotropy. Furthermore, to identify and evaluate possible drug targets, we conducted a thorough search within the Drug-Gene Interaction Database (DGIdb).</div></div><div><h3>Results</h3><div>Analysis using MR unveiled significant and causative associations between genetically determined CASP-8 (odds ratio (OR): 0.97), CD40 (OR: 0.96), IL-18 (OR: 0.98), SLAMF1 (OR: 0.97), and uPA (OR: 0.98) with MDD. Conversely, reverse MR analysis indicated causal associations between MDD and CCL19 (OR: 1.15), HGF (OR: 1.15), IL-8 (OR: 1.10), IL-18 (OR: 1.11), IL20RA (OR: 1.12), TGFA (OR: 1.12) and TNFSF14 (OR: 1.16). Notably, a significant bidirectional causal link was observed between IL-18 and MDD. Gene-drug analysis identified CD40, HGF, IL-8, IL-18, SLAMF1, and TGFA as potential therapeutic targets.</div></div><div><h3>Conclusions</h3><div>We've pinpointed causal links between inflammation-related proteins and MDD, offering compelling and innovative evidence to enhance our understanding of the inflammatory mechanisms involved in MDD and to investigate potential targets for anti-MDD medications.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111165"},"PeriodicalIF":5.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melanin-concentrating hormone promotes feeding through the lateral septum","authors":"Mikayla A. Payant,&nbsp;Anjali Shankhatheertha,&nbsp;Melissa J. Chee","doi":"10.1016/j.pnpbp.2024.111163","DOIUrl":"10.1016/j.pnpbp.2024.111163","url":null,"abstract":"<div><div>Feeding is necessary for survival but can be hindered by anxiety or fear, thus neural systems that can regulate anxiety states are key to elucidating the expression of food-related behaviors. Melanin-concentrating hormone (MCH) is a neuropeptide produced in the lateral hypothalamus and zona incerta that promotes feeding and anxiogenesis. The orexigenic actions of MCH that prolong ongoing homeostatic or hedonic feeding are context-dependent and more prominent in male than female rodents, but it is not clear where MCH acts to initiate feeding. The lateral septum (LS) promotes feeding and suppresses anxiogenesis when inhibited, and it comprises the densest projections from MCH neurons. However, it is not known whether the LS is a major contributor to MCH-mediated feeding. As MCH inhibits LS cells by MCH receptor (MCHR1) activation, MCH may promote feeding via the LS. We bilaterally infused MCH into the LS and found that MCH elicited a rapid and long-lasting increase in the consumption of standard chow and a palatable, high sugar diet in male and female mice; these MCH effects were blocked by the co-administration of a MCHR1 antagonist TC- MCH 7c. Interestingly, the orexigenic effect of MCH was abolished in a novel, anxiogenic environment even when presented with a food reward, but MCH did not induce anxiety-like behaviors. These findings indicated the LS as a novel region underlying orexigenic MCH actions, which stimulated and enhanced feeding in both sexes in a context -dependent manner that was most prominent in the homecage.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111163"},"PeriodicalIF":5.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142402002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of muscarinic acetylcholine receptor-mediated cholinergic neurotransmission in TMS–EEG responses","authors":"Yufei Song ,&nbsp;Pedro C. Gordon ,&nbsp;Olivier Roy ,&nbsp;Johanna Metsomaa ,&nbsp;Paolo Belardinelli ,&nbsp;Maryam Rostami ,&nbsp;Ulf Ziemann","doi":"10.1016/j.pnpbp.2024.111167","DOIUrl":"10.1016/j.pnpbp.2024.111167","url":null,"abstract":"<div><div>The combination of transcranial magnetic stimulation and electroencephalography (TMS–EEG) is emerging as a valuable tool for investigating brain functions in health and disease. However, the detailed neural mechanisms underlying TMS–EEG responses, including TMS-evoked EEG potentials (TEPs) and TMS-induced EEG oscillations (TIOs), remain largely unknown. Combining TMS–EEG with pharmacological interventions provides a unique opportunity to elucidate the roles of specific receptor-mediated neurotransmissions in these responses. Here, we investigated the involvement of muscarinic acetylcholine receptor (mAChR)-mediated cholinergic neurotransmission in TMS–EEG responses by evaluating the effects of mAChR antagonists on TEPs and TIOs in twenty-four healthy participants using a randomized, placebo-controlled crossover design. TEPs and TIOs were measured before and after administering a single oral dose of scopolamine (a non-selective mAChR antagonist), biperiden (an M1 mAChR antagonist), or placebo, with TMS targeting the left medial prefrontal cortex (mPFC), angular gyrus (AG), and supplementary motor area (SMA). The results indicated that mAChR-mediated cholinergic neurotransmission played a role in TEPs, but not TIOs, in a target-specific manner. Specifically, scopolamine significantly increased the amplitude of a local TEP component between approximately 40 and 63 ms post-stimulus when TMS was applied to the SMA, but not the mPFC or AG. Biperiden produced a similar but less pronounced effect. Importantly, the effects of these mAChR antagonists on TEPs were independent of those on sensory-evoked EEG potentials caused by TMS-associated sensory stimulation. These findings expand our understanding of TMS–EEG physiology, providing insights for its application in physiological and clinical research.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111167"},"PeriodicalIF":5.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emotional dysregulation following prenatal stress is associated with altered prefrontal cortex responsiveness to an acute challenge in adolescence","authors":"Rodrigo Orso ,&nbsp;Kerstin Camile Creutzberg ,&nbsp;Veronica Begni ,&nbsp;Giulia Petrillo ,&nbsp;Annamaria Cattaneo ,&nbsp;Marco Andrea Riva","doi":"10.1016/j.pnpbp.2024.111162","DOIUrl":"10.1016/j.pnpbp.2024.111162","url":null,"abstract":"<div><div>Exposure to prenatal stress (PNS) has the potential to elicit multiple neurobiological alterations and increase the susceptibility to psychiatric disorders. Moreover, gestational stress may sensitize the brain toward an altered response to subsequent challenges. Here, we investigated the effects of PNS in rats and assessed whether these animals exhibit an altered brain responsiveness to an acute stress (AS) during adolescence. From gestational day 14 until delivery, Sprague Dawley dams were exposed to PNS or left undisturbed. During adolescence (PND38 to PND41), offspring were tested in the social interaction and splash test. At PND44 half of the animals were exposed to 5 min of forced swim stress. Males and Females exposed to PNS showed reduced sociability and increased anhedonic-like behavior. At the molecular level, exposure of adolescent rats to AS produced increased activation of the amygdala and ventral and dorsal hippocampus. Regarding the prefrontal cortex (PFC), we observed a pronounced activation in PNS males exposed to AS. Cell-type specific transcriptional analyses revealed a significant imbalance in the activation of PFC excitatory and inhibitory neurons in PNS males and females exposed to AS. Furthermore, stressed males exhibited disrupted HPA-axis function, while females showed impairments in the modulation of antioxidant genes. Our study shows that PNS induces emotional dysregulation and alters the responsiveness of the PFC to an acute stressor. Moreover, the disruption of excitatory and inhibitory balance during adolescence could influence the ability to respond to challenging events that may contribute to precipitate a full-blown pathologic condition.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111162"},"PeriodicalIF":5.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between cytokine levels and cognitive function among individuals at clinical high risk for psychosis","authors":"Tian Hong Zhang ,&nbsp;Xing Chen ,&nbsp;Yan Yan Wei ,&nbsp;Xiao Chen Tang ,&nbsp;Li Hua Xu ,&nbsp;Hui Ru Cui ,&nbsp;Hai Chun Liu ,&nbsp;Zi Xuan Wang ,&nbsp;Tao Chen ,&nbsp;Chun Bo Li ,&nbsp;Ji Jun Wang","doi":"10.1016/j.pnpbp.2024.111166","DOIUrl":"10.1016/j.pnpbp.2024.111166","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the intricate interplay among cytokines, cognitive functioning, and conversion to psychosis in individuals at clinical high-risk (CHR) for psychosis.</div></div><div><h3>Method</h3><div>We initially enrolled 385 individuals at CHR and 95 healthy controls (HCs). Subsequently, 102 participants at CHR completed the 1-year follow-up assessments, and 47 participants transitioned to psychosis. We assessed the levels of interleukins (IL-1β, IL-2, IL-6, IL-8, IL-10), tumor necrosis factor-α (TNF-α), granulocyte-macrophage colony-stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF). We comprehensively evaluated cognitive performance across six domains, including speed of processing (SP), attention/vigilance (AV), working memory (WM), verbal learning (VeL), visual learning (ViL), and reasoning and problem-solving (RPS).</div></div><div><h3>Results</h3><div>Higher baseline cognitive domain scores were associated with elevated GM-CSF and reduced VEGF levels. In the follow-up analysis, significant time effects were observed for IL-1β and IL-2. We also observed significant interaction effects between specific cognitive domains (AV, WM, VeL, and OCS) and levels of cytokine (GM-CSF, IL-1β, IL-6, and TNF-α). Changes in WM were negatively correlated with changes in TNF-α levels and positively correlated with changes in VEGF levels. Variations in VeL were inversely correlated with changes in GM-CSF and IL-10 levels, whereas changes in RPS were positively associated with changes in GM-CSF and IL-8 levels.</div></div><div><h3>Conclusions</h3><div>Our results revealed intricate associations among cytokine levels, cognitive performance, and psychosis progression.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111166"},"PeriodicalIF":5.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142395281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying genetic variants associated with side effects of antidepressant treatment: A systematic review","authors":"Gabriel da Rocha Zurchimitten ,&nbsp;Laísa Camerini ,&nbsp;Geison Souza Izídio ,&nbsp;Gabriele Ghisleni","doi":"10.1016/j.pnpbp.2024.111154","DOIUrl":"10.1016/j.pnpbp.2024.111154","url":null,"abstract":"<div><div>Major Depressive Disorder (MDD) is one of the most prevalent neurobiological disorders globally. Antidepressant medications are the first-line treatment for managing symptoms. However, over time, pharmacotherapy has been linked to several challenges, primarily due to the wide array of side effects that often reduce patient adherence to treatment. The literature suggests that these side effects may be influenced by polymorphisms in genes related to the pharmacokinetics and pharmacodynamics of antidepressants. Thus, this systematic review aimed to identify studies that investigated the association between genetic variants and side effects resulting from antidepressant treatment in individuals with MDD. Original articles indexed in the electronic databases Cochrane Library, EMBASE, MEDLINE via PubMed, and Scopus were identified. A total of 55 studies were included in the review, and data regarding the outcomes of interest were extracted. Due to the exploratory nature of the review, a narrative/descriptive synthesis of the results was performed. The risk of bias was evaluated using the Joanna Briggs Institute's tools, tailored to the design of each study. Polymorphisms in 35 genes were statistically associated with the development of side effects. A subsequent Protein-Protein Interaction Network analysis helped elucidate the key biological pathways involved in antidepressant side effects, with a view toward exploring the potential application of pharmacogenetic markers in clinical practice.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111154"},"PeriodicalIF":5.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antidepressants account for the causal effect of major depressive disorder on type 2 diabetes","authors":"Ancha Baranova ,&nbsp;Dongming Liu ,&nbsp;Wenxi Sun ,&nbsp;Chenxin Xu ,&nbsp;Miao Chen ,&nbsp;Hongbao Cao ,&nbsp;Fuquan Zhang","doi":"10.1016/j.pnpbp.2024.111164","DOIUrl":"10.1016/j.pnpbp.2024.111164","url":null,"abstract":"<div><h3>Background</h3><div>Patients with major depressive disorder (MDD) face an elevated risk of type 2 diabetes (T2D). However, the contribution of the disease itself versus the side effects of antidepressants to this increased risk remains unclear.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the overall and independent effects of MDD and exposure to antidepressants on T2D risk.</div></div><div><h3>Methods</h3><div>Summary genome-wide association study datasets were utilized for the Mendelian randomization (MR) and multivariable MR (MVMR) analyses, including ones for MDD (<em>N</em> = 500,199), antidepressants (<em>N</em> = 175,161), and T2D (<em>N</em> = 933,970). Bayesian colocalization analysis was used to reveal shared genetic variation between MDD, antidepressants, and T2D.</div></div><div><h3>Results</h3><div>We found that both MDD (OR: 1.15, CI: 1.03–1.30, <em>P</em> = 0.016) and antidepressants (OR: 1.37, CI: 1.22–1.53, <em>P</em> = 2.75E-08) have overall causal effects on T2D. While T2D was associated with the risk of antidepressant use (OR: 1.08, CI: 1.06–1.11, <em>P</em> = 8.80E-10), but not with the risk of MDD (OR: 1.00, CI: 0.98–1.01, <em>P</em> = 0.661). Our MVMR analysis showed that the use of antidepressants is associated with higher risks of T2D (OR: 1.21, CI: 1.07–1.37, <em>P</em> = 7.19E-04), while MDD is not linked to the risk of T2D (OR: 1.01, CI: 0.86–1.18, <em>P</em> = 0.799). Colocalization analysis identified two shared genetic loci between antidepressants and T2D.</div></div><div><h3>Conclusions</h3><div>The elevated T2D risk in MDD patients is chiefly caused by antidepressant use. These findings emphasize the importance of considering the impact of antidepressants on metabolic health in individuals with MDD.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111164"},"PeriodicalIF":5.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Allopregnanolone and intrusive memories: A potential therapeutic target for PTSD treatment?","authors":"Khalisa Amir Hamzah,&nbsp;Ottmar V. Lipp,&nbsp;Luke J. Ney","doi":"10.1016/j.pnpbp.2024.111168","DOIUrl":"10.1016/j.pnpbp.2024.111168","url":null,"abstract":"<div><div>Significant amounts of research have been devoted to treatment of post-traumatic stress disorder (PTSD) and the understanding of its fear and stress-related symptoms. However, current interventions are only effective in 60 % of the patient population. Allopregnanolone has become a topic of interest for PTSD due to its influences on inhibitory neurotransmission and the physiological stress response. This review explores available literature that suggests that allopregnanolone has an influence on (a) chronic stress and anxiety-like symptoms, (b) fear conditioning and contextual fear, and (c) intrusive and emotional memories. A relationship between allopregnanolone and PTSD is suggested, postulating that allopregnanolone is a potential target for the treatment of PTSD. This very exciting prospect calls for the expansion of research investigating a direct relationship between allopregnanolone and PTSD.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"136 ","pages":"Article 111168"},"PeriodicalIF":5.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}