Sulcal pits, defined as the deepest points of the cortical surface and identified as stable landmarks, exhibit a consistent emergence sequence that aligns with established gyrification patterns, underscoring their potential as markers for early neurodevelopmental trajectories. Here, we investigate the potential of sulcal pits in characterizing the etiological roots of neurodevelopmental traits and disorders.
This systematic review (PROSPERO register: CRD42022347303) was conducted according to PRISMA guidelines. Searches were performed in PubMed, Web of Science (WOS), and Scopus, initially identifying 102 articles, from which 53 were screened and 19 finally included. The articles were categorized into two main groups: those exploring the ontogenetic processes of sulcal pits and those investigating their relationship with neurodevelopmental phenotypes in health and disease.
The review findings indicate that individuals with congenital conditions or neurodevelopmental disorders exhibit distinct patterns of sulcal pits that correlate with cognitive traits. Additionally, graph analyses consistently show lower mean similarity within individuals from affected groups, suggesting that variations in sulcal pit patterns reflect the impact of neurodevelopmental disturbances.
These results highlight the potential of sulcal pits to capture instabilities in early brain development. However, they also point to a lack of comprehensive biological interpretation in the current literature. Further research is needed to enhance our understanding of the significance of sulcal pits in neurodevelopmental outcomes and to advance their use as diagnostic tools.
{"title":"The sulcal pits as neurodevelopmental markers: A systematic review about their potential use in clinical practice","authors":"Noemí Hostalet , Pilar Salgado-Pineda , Neus Martínez-Abadías , Mar Fatjó-Vilas","doi":"10.1016/j.pnpbp.2025.111289","DOIUrl":"10.1016/j.pnpbp.2025.111289","url":null,"abstract":"<div><div>Sulcal pits, defined as the deepest points of the cortical surface and identified as stable landmarks, exhibit a consistent emergence sequence that aligns with established gyrification patterns, underscoring their potential as markers for early neurodevelopmental trajectories. Here, we investigate the potential of sulcal pits in characterizing the etiological roots of neurodevelopmental traits and disorders.</div><div>This systematic review (PROSPERO register: CRD42022347303) was conducted according to PRISMA guidelines. Searches were performed in PubMed, Web of Science (WOS), and Scopus, initially identifying 102 articles, from which 53 were screened and 19 finally included. The articles were categorized into two main groups: those exploring the ontogenetic processes of sulcal pits and those investigating their relationship with neurodevelopmental phenotypes in health and disease.</div><div>The review findings indicate that individuals with congenital conditions or neurodevelopmental disorders exhibit distinct patterns of sulcal pits that correlate with cognitive traits. Additionally, graph analyses consistently show lower mean similarity within individuals from affected groups, suggesting that variations in sulcal pit patterns reflect the impact of neurodevelopmental disturbances.</div><div>These results highlight the potential of sulcal pits to capture instabilities in early brain development. However, they also point to a lack of comprehensive biological interpretation in the current literature. Further research is needed to enhance our understanding of the significance of sulcal pits in neurodevelopmental outcomes and to advance their use as diagnostic tools.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111289"},"PeriodicalIF":5.3,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143384004","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}
Pub Date : 2025-02-07DOI: 10.1016/j.pnpbp.2025.111288
Mauro Scala , María del Rocío González Soltero , Alberto Bellido Esteban , José Miguel Biscaia Fernández , Verónica Romero-Ferreiro , Alessandro Serretti , Giuseppe Fanelli , Roberto Rodriguez-Jimenez
Backgrounds
Oropharyngeal microbiota may be implicated in the onset and progression of psychotic disorders. This scoping review aims to map the existing evidence concerning the composition, diversity, and metabolic pathways of the oropharyngeal microbiota in patients aged 18 to 65 with a main diagnosis of a psychotic disorder, including individuals at clinical high-risk for psychosis (CHRP) or experiencing first episode psychosis (FEP).
Methods
The scoping review was performed according to the PRISMA-ScR checklist. The systematic literature search was conducted using PubMed, Web of Science, and CINAHL until February 2024.
Results
Seven cross-sectional studies were included, comprising 43 individuals at CHRP, 13 with FEP, 85 with first-episode of schizophrenia (FES), 171 with schizophrenia, and 8 with another schizophrenia spectrum disorder. The oropharyngeal microbiota showed an increase in Lactobacillus gasseri abundance in schizophrenia, and in Firmicutes/Proteobacteria phylum ratio in patients experiencing CHR-P and FES. In schizophrenia, an altered β-diversity was observed alongside increased metabolic pathways related to metabolite transporters. In FES, higher α-diversity and disruptions in amino acid, carbohydrate, and xenobiotic metabolism pathways were found. Hydrogen sulfide (H2S)-producing bacteria were generally enriched in all the stages of disease. Correlations were observed between oropharyngeal microbiota and psychotic symptom domains.
Conclusions
Potential microbial signatures, such as Lactobacillus gasseri and H2S-producing bacteria, were identified in the oropharyngeal microbiota. Alterations in the oropharyngeal microbiota composition and function may be associated with different stages of psychotic disorders, with some overlap between CHR-P and FES.
{"title":"Oropharyngeal microbiota in patients with psychotic disorders: A scoping review on compositional and functional alterations","authors":"Mauro Scala , María del Rocío González Soltero , Alberto Bellido Esteban , José Miguel Biscaia Fernández , Verónica Romero-Ferreiro , Alessandro Serretti , Giuseppe Fanelli , Roberto Rodriguez-Jimenez","doi":"10.1016/j.pnpbp.2025.111288","DOIUrl":"10.1016/j.pnpbp.2025.111288","url":null,"abstract":"<div><h3>Backgrounds</h3><div>Oropharyngeal microbiota may be implicated in the onset and progression of psychotic disorders. This scoping review aims to map the existing evidence concerning the composition, diversity, and metabolic pathways of the oropharyngeal microbiota in patients aged 18 to 65 with a main diagnosis of a psychotic disorder, including individuals at clinical high-risk for psychosis (CHR<img>P) or experiencing first episode psychosis (FEP).</div></div><div><h3>Methods</h3><div>The scoping review was performed according to the PRISMA-ScR checklist. The systematic literature search was conducted using PubMed, Web of Science, and CINAHL until February 2024.</div></div><div><h3>Results</h3><div>Seven cross-sectional studies were included, comprising 43 individuals at CHR<img>P, 13 with FEP, 85 with first-episode of schizophrenia (FES), 171 with schizophrenia, and 8 with another schizophrenia spectrum disorder. The oropharyngeal microbiota showed an increase in <em>Lactobacillus gasseri</em> abundance in schizophrenia, and in <em>Firmicutes/Proteobacteria</em> phylum ratio in patients experiencing CHR-P and FES. In schizophrenia, an altered β-diversity was observed alongside increased metabolic pathways related to metabolite transporters. In FES, higher α-diversity and disruptions in amino acid, carbohydrate, and xenobiotic metabolism pathways were found. Hydrogen sulfide (H<sub>2</sub>S)-producing bacteria were generally enriched in all the stages of disease. Correlations were observed between oropharyngeal microbiota and psychotic symptom domains.</div></div><div><h3>Conclusions</h3><div>Potential microbial signatures, such as <em>Lactobacillus gasseri</em> and H<sub>2</sub>S-producing bacteria, were identified in the oropharyngeal microbiota. Alterations in the oropharyngeal microbiota composition and function may be associated with different stages of psychotic disorders, with some overlap between CHR-P and FES.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111288"},"PeriodicalIF":5.3,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383980","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}
Major depressive disorder (MDD) and bipolar disorder (BD) share various clinical behaviors and have confounded clinical diagnoses. Converging studies have suggested MDD and BD as disorders with abnormal communication among functional brain networks involved in mental activity and redirection. However, whether MDD and BD show disease-specific alterations in network information interaction remains unclear. This study collected resting-state functional MRI data of 98 patients with MDD, 55 patients with BD, and sex-, age-, and education-matched 95 healthy controls. Spectral dynamic causal model (spDCM) was used to investigate effective connectivities among three large-scale intrinsic functional networks including the default mode network (DMN), salience network (SN), and dorsal attention network (DAN). Effective connectivities showing disease-specific changes were then used as input features of support vector models to predict clinical symptoms and classify individuals with MDD and BD. Compared with healthy controls, both the MDD and BD groups showed increased DAN → SN connectivity. However, within-network connectivities of DMN and DAN showed opposite effects on the diseases. Notably, MDD and BD also showed different alterations on a connectivity loop of SN → DAN → DMN → SN, which could be used to predict the clinical symptom severity of either MDD or BD. Individuals with MDD and BD could be further classified by using connectivities showing opposite disease effects. Our findings reveal common and unique alterations of network interactions in MDD and BD, and further suggest disease-specific neuroimaging markers for clinical diagnosis.
{"title":"Disease-specific alterations of effective connectivity across anti-correlated networks in major depressive disorder and bipolar disorder","authors":"Yun-Shuang Fan , Saike Zhang , Wei Sheng , Jing Guo , Hezong Ling , Qian Cui , Wei Huang , Huafu Chen","doi":"10.1016/j.pnpbp.2025.111283","DOIUrl":"10.1016/j.pnpbp.2025.111283","url":null,"abstract":"<div><div>Major depressive disorder (MDD) and bipolar disorder (BD) share various clinical behaviors and have confounded clinical diagnoses. Converging studies have suggested MDD and BD as disorders with abnormal communication among functional brain networks involved in mental activity and redirection. However, whether MDD and BD show disease-specific alterations in network information interaction remains unclear. This study collected resting-state functional MRI data of 98 patients with MDD, 55 patients with BD, and sex-, age-, and education-matched 95 healthy controls. Spectral dynamic causal model (spDCM) was used to investigate effective connectivities among three large-scale intrinsic functional networks including the default mode network (DMN), salience network (SN), and dorsal attention network (DAN). Effective connectivities showing disease-specific changes were then used as input features of support vector models to predict clinical symptoms and classify individuals with MDD and BD. Compared with healthy controls, both the MDD and BD groups showed increased DAN → SN connectivity. However, within-network connectivities of DMN and DAN showed opposite effects on the diseases. Notably, MDD and BD also showed different alterations on a connectivity loop of SN → DAN → DMN → SN, which could be used to predict the clinical symptom severity of either MDD or BD. Individuals with MDD and BD could be further classified by using connectivities showing opposite disease effects. Our findings reveal common and unique alterations of network interactions in MDD and BD, and further suggest disease-specific neuroimaging markers for clinical diagnosis.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111283"},"PeriodicalIF":5.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374650","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}
Pub Date : 2025-02-05DOI: 10.1016/j.pnpbp.2025.111284
Pin Wang , Heya Luan , Shaoqi Li , Xiaodong Han , Wenxian Sun , Jin Gong , Chang Xu , Runqi Chen , Cuibai Wei
Background
Extensive perivascular spaces (PVS) burden has been reported to be associated with neurodegenerative diseases and brain structure; however, the causal effects has not been determined yet. Therefore, this study aimed to investigate the causal effect of extensive PVS burden on neurodegenerative diseases and brain structure through Mendelian randomization (MR) analysis.
Methods
Two-sample bidirectional MR was conducted based on publicly available genome-wide association studies (GWAS) summary statistics. Causal estimates of extensive PVS burden on neurodegenerative diseases and brain structure were primarily assessed using the inverse-variance weighted (IVW) method, supplemented by additional methods, including MR-Egger, weighted median, simple mode, and weighted mode. Sensitivity analyses were performed to assess heterogeneity and pleiotropy. In addition, we explored whether brain structure act as a mediating factor in the pathway from extensive PVS burden to neurodegenerative diseases.
Results
Our MR study found that extensive PVS burden in white matter (WM-PVS) burden was associated with lower Alzheimer's disease (AD) risk (IVW OR (95 % CI) = 0.963(0.929 to 0.999), P = 0.0428), with no heterogeneity and pleiotropy detected. In addition, following FDR correction, we found bidirectional causal relationships between extensive PVS burden and brain structure. Moreover, our results of the mediated analysis showed that the surface area of parahippocampal, as a mediating variable, plays an important role in the causal relationship between WM-PVS and AD. The mediation effect is 18 %.
Conclusions
Our study provides evidence for the causal associations of different extensive PVS burden phenotypes with neurodegenerative diseases and brain structures, improving our understanding of the complex relationships between different brain injuries.
{"title":"Extensive perivascular spaces burden causally affects neurodegenerative diseases and brain structure: A two-sample bidirectional Mendelian randomization study","authors":"Pin Wang , Heya Luan , Shaoqi Li , Xiaodong Han , Wenxian Sun , Jin Gong , Chang Xu , Runqi Chen , Cuibai Wei","doi":"10.1016/j.pnpbp.2025.111284","DOIUrl":"10.1016/j.pnpbp.2025.111284","url":null,"abstract":"<div><h3>Background</h3><div>Extensive perivascular spaces (PVS) burden has been reported to be associated with neurodegenerative diseases and brain structure; however, the causal effects has not been determined yet. Therefore, this study aimed to investigate the causal effect of extensive PVS burden on neurodegenerative diseases and brain structure through Mendelian randomization (MR) analysis.</div></div><div><h3>Methods</h3><div>Two-sample bidirectional MR was conducted based on publicly available genome-wide association studies (GWAS) summary statistics. Causal estimates of extensive PVS burden on neurodegenerative diseases and brain structure were primarily assessed using the inverse-variance weighted (IVW) method, supplemented by additional methods, including MR-Egger, weighted median, simple mode, and weighted mode. Sensitivity analyses were performed to assess heterogeneity and pleiotropy. In addition, we explored whether brain structure act as a mediating factor in the pathway from extensive PVS burden to neurodegenerative diseases.</div></div><div><h3>Results</h3><div>Our MR study found that extensive PVS burden in white matter (WM-PVS) burden was associated with lower Alzheimer's disease (AD) risk (IVW OR (95 % CI) = 0.963(0.929 to 0.999), <em>P</em> = 0.0428), with no heterogeneity and pleiotropy detected. In addition, following FDR correction, we found bidirectional causal relationships between extensive PVS burden and brain structure. Moreover, our results of the mediated analysis showed that the surface area of parahippocampal, as a mediating variable, plays an important role in the causal relationship between WM-PVS and AD. The mediation effect is 18 %.</div></div><div><h3>Conclusions</h3><div>Our study provides evidence for the causal associations of different extensive PVS burden phenotypes with neurodegenerative diseases and brain structures, improving our understanding of the complex relationships between different brain injuries.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111284"},"PeriodicalIF":5.3,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143348783","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}
Pub Date : 2025-02-03DOI: 10.1016/j.pnpbp.2025.111279
Zhen Xuen Brandon Low , Shin Jie Yong , Hayam A. Alrasheed , Maha F. Al-Subaie , Nawal A. Al Kaabi , Mubarak Alfaresi , Hawra Albayat , Jawaher Alotaibi , Ali Al Bshabshe , Ameen S.S. Alwashmi , Amal A. Sabour , Maha A. Alshiekheid , Zainab H. Almansour , Huda Alharthi , Hani A. Al Ali , Adel A. Almoumen , Nabil A. Alqasimi , Hajir AlSaihati , Alfonso J. Rodriguez-Morales , Ali A. Rabaan
Rationale
In our ongoing battle against the coronavirus 2019 (COVID-19) pandemic, a major challenge is the enduring symptoms that continue after acute infection. Also known as Long COVID, post-COVID-19 syndrome (PCS) often comes with debilitating symptoms like fatigue, disordered sleep, olfactory dysfunction, and cognitive issues (“brain fog”). Currently, there are no approved treatments for PCS. Recent research has uncovered that the severity of PCS is inversely linked to circulating serotonin levels, highlighting the potential of serotonin-modulating therapeutics for PCS. Therefore, we propose that serotonergic psychedelics, acting mainly via the 5-HT2A serotonin receptor, hold promise for treating PCS.
Objectives
Our review aims to elucidate potential mechanisms by which serotonergic psychedelics may alleviate the symptoms of PCS.
Results
Potential mechanisms through which serotonergic psychedelics may alleviate PCS symptoms are discussed, with emphasis on their effects on inflammation, neuroplasticity, and gastrointestinal function. Additionally, this review explores the potential of serotonergic psychedelics in mitigating endothelial dysfunction, a pivotal aspect of PCS pathophysiology implicated in organ dysfunction. This review also examines the potential role of serotonergic psychedelics in alleviating specific PCS symptoms, which include olfactory dysfunction, cognitive impairment, sleep disturbances, and mental health challenges.
Conclusions
Emerging evidence suggests that serotonergic psychedelics may alleviate PCS symptoms. However, further high-quality research is needed to thoroughly assess their safety and efficacy in treating patients with PCS.
{"title":"Serotonergic psychedelics as potential therapeutics for post-COVID-19 syndrome (or Long COVID): A comprehensive review","authors":"Zhen Xuen Brandon Low , Shin Jie Yong , Hayam A. Alrasheed , Maha F. Al-Subaie , Nawal A. Al Kaabi , Mubarak Alfaresi , Hawra Albayat , Jawaher Alotaibi , Ali Al Bshabshe , Ameen S.S. Alwashmi , Amal A. Sabour , Maha A. Alshiekheid , Zainab H. Almansour , Huda Alharthi , Hani A. Al Ali , Adel A. Almoumen , Nabil A. Alqasimi , Hajir AlSaihati , Alfonso J. Rodriguez-Morales , Ali A. Rabaan","doi":"10.1016/j.pnpbp.2025.111279","DOIUrl":"10.1016/j.pnpbp.2025.111279","url":null,"abstract":"<div><h3>Rationale</h3><div>In our ongoing battle against the coronavirus 2019 (COVID-19) pandemic, a major challenge is the enduring symptoms that continue after acute infection. Also known as Long COVID, post-COVID-19 syndrome (PCS) often comes with debilitating symptoms like fatigue, disordered sleep, olfactory dysfunction, and cognitive issues (“brain fog”). Currently, there are no approved treatments for PCS. Recent research has uncovered that the severity of PCS is inversely linked to circulating serotonin levels, highlighting the potential of serotonin-modulating therapeutics for PCS. Therefore, we propose that serotonergic psychedelics, acting mainly via the 5-HT2A serotonin receptor, hold promise for treating PCS.</div></div><div><h3>Objectives</h3><div>Our review aims to elucidate potential mechanisms by which serotonergic psychedelics may alleviate the symptoms of PCS.</div></div><div><h3>Results</h3><div>Potential mechanisms through which serotonergic psychedelics may alleviate PCS symptoms are discussed, with emphasis on their effects on inflammation, neuroplasticity, and gastrointestinal function. Additionally, this review explores the potential of serotonergic psychedelics in mitigating endothelial dysfunction, a pivotal aspect of PCS pathophysiology implicated in organ dysfunction. This review also examines the potential role of serotonergic psychedelics in alleviating specific PCS symptoms, which include olfactory dysfunction, cognitive impairment, sleep disturbances, and mental health challenges.</div></div><div><h3>Conclusions</h3><div>Emerging evidence suggests that serotonergic psychedelics may alleviate PCS symptoms. However, further high-quality research is needed to thoroughly assess their safety and efficacy in treating patients with PCS.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111279"},"PeriodicalIF":5.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257404","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}
Pub Date : 2025-02-03DOI: 10.1016/j.pnpbp.2025.111280
Hongling Guo , Tahir Ali , Shupeng Li
Major depressive disorder (MDD), also known as depression, is a prevalent mental disorder that leads to severe disease burden worldwide. Over the past two decades, significant progress has been made in understanding the pathogenesis and developing novel treatments for MDD. Among the complicated etiologies of MDD, chronic stress is a major risk factor. Exploring the underlying brain circuit mechanisms of chronic stress regulation has been an area of active research for recent years. A growing body of preclinical and clinical research has revealed that abnormalities in the brain circuits are closely associated with failures in coping with stress in depressed individuals. Nevertheless, neural circuit mechanisms underlying chronic stress processing and the onset of depression remain a major puzzle. Here, we review recent literature focusing on circuit- and cell-type-specific dissection of depression-like behaviors in chronic stress-related animal models of MDD and outline the key questions.
{"title":"Neural circuits mediating chronic stress: Implications for major depressive disorder","authors":"Hongling Guo , Tahir Ali , Shupeng Li","doi":"10.1016/j.pnpbp.2025.111280","DOIUrl":"10.1016/j.pnpbp.2025.111280","url":null,"abstract":"<div><div>Major depressive disorder (MDD), also known as depression, is a prevalent mental disorder that leads to severe disease burden worldwide. Over the past two decades, significant progress has been made in understanding the pathogenesis and developing novel treatments for MDD. Among the complicated etiologies of MDD, chronic stress is a major risk factor. Exploring the underlying brain circuit mechanisms of chronic stress regulation has been an area of active research for recent years. A growing body of preclinical and clinical research has revealed that abnormalities in the brain circuits are closely associated with failures in coping with stress in depressed individuals. Nevertheless, neural circuit mechanisms underlying chronic stress processing and the onset of depression remain a major puzzle. Here, we review recent literature focusing on circuit- and cell-type-specific dissection of depression-like behaviors in chronic stress-related animal models of MDD and outline the key questions.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111280"},"PeriodicalIF":5.3,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143200846","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}
Pub Date : 2025-02-02DOI: 10.1016/j.pnpbp.2025.111281
Valentín Cabrera , Paula Abate , Verónica Balaszczuk , Ana Fabiola Macchione
Alcohol consumption is a worldwide concern that causes 5 % of the global disease burden and contributes to 3 million deaths per year. Several studies suggest an increase in alcohol drinking and alcohol related problems. Alcohol Use Disorder (formerly referred as alcoholism or alcohol addiction) is one of many possible outcomes of an early and prolonged alcohol consumption and it is highly comorbid with anxiety disorders, impulsivity and memory deficits among others. In this review we approach recent data about global and American prevalence of alcohol use and discuss different factors that contribute to alcohol consumption. Furthermore, we revise evidence of ethanol effects on anxiety-like behaviors, impulsivity and spatial memory. Lastly, we look at the Omega-3 fatty acid as a possible course of action in mitigating the aforementioned deleterious effects of alcohol consumption.
{"title":"Alcohol outcomes on anxiety, impulsivity and spatial memory: Possible Omega-3 amelioration effects","authors":"Valentín Cabrera , Paula Abate , Verónica Balaszczuk , Ana Fabiola Macchione","doi":"10.1016/j.pnpbp.2025.111281","DOIUrl":"10.1016/j.pnpbp.2025.111281","url":null,"abstract":"<div><div>Alcohol consumption is a worldwide concern that causes 5 % of the global disease burden and contributes to 3 million deaths per year. Several studies suggest an increase in alcohol drinking and alcohol related problems. Alcohol Use Disorder (formerly referred as alcoholism or alcohol addiction) is one of many possible outcomes of an early and prolonged alcohol consumption and it is highly comorbid with anxiety disorders, impulsivity and memory deficits among others. In this review we approach recent data about global and American prevalence of alcohol use and discuss different factors that contribute to alcohol consumption. Furthermore, we revise evidence of ethanol effects on anxiety-like behaviors, impulsivity and spatial memory. Lastly, we look at the Omega-3 fatty acid as a possible course of action in mitigating the aforementioned deleterious effects of alcohol consumption.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111281"},"PeriodicalIF":5.3,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143191446","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}
Pub Date : 2025-01-31DOI: 10.1016/j.pnpbp.2025.111278
Junia Lara de Deus , Juliana Marino Maia , Renato Nery Soriano , Mateus R. Amorim , Luiz G.S. Branco
Neuroinflammation is a critical factor in the pathogenesis of various neurodegenerative and psychiatric disorders, including Alzheimer's disease, Parkinson's disease, and major depressive disorder. Psychedelics, such as psilocybin, lysergic acid diethylamide (LSD), and dimethyltryptamine (DMT), have demonstrated promising therapeutic effects on neuroinflammation, primarily through interactions with serotonin (5-HT) receptors, particularly the 5-HT2A receptor. Activation of these receptors by psychedelics modulates the production of pro-inflammatory cytokines, regulates microglial activity, and shifts the balance between neurotoxic and neuroprotective metabolites. Additionally, psychedelics affect critical signaling pathways, including the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), and mechanistic target of rapamycin (mTOR) pathways, promoting neuroplasticity and exerting anti-inflammatory effects. Beyond the serotonergic system, other neurotransmitter systems—including the glutamatergic, dopaminergic, noradrenergic, gamma-aminobutyric acid (GABAergic), and cholinergic systems—also play significant roles in mediating the effects of psychedelics. This review examines the intricate mechanisms by which psychedelics modulate neuroinflammation and underscores their potential as innovative therapeutic agents for treating neuroinflammatory and neuropsychiatric disorders.
{"title":"Psychedelics in neuroinflammation: Mechanisms and therapeutic potential","authors":"Junia Lara de Deus , Juliana Marino Maia , Renato Nery Soriano , Mateus R. Amorim , Luiz G.S. Branco","doi":"10.1016/j.pnpbp.2025.111278","DOIUrl":"10.1016/j.pnpbp.2025.111278","url":null,"abstract":"<div><div>Neuroinflammation is a critical factor in the pathogenesis of various neurodegenerative and psychiatric disorders, including Alzheimer's disease, Parkinson's disease, and major depressive disorder. Psychedelics, such as psilocybin, lysergic acid diethylamide (LSD), and dimethyltryptamine (DMT), have demonstrated promising therapeutic effects on neuroinflammation, primarily through interactions with serotonin (5-HT) receptors, particularly the 5-HT2A receptor. Activation of these receptors by psychedelics modulates the production of pro-inflammatory cytokines, regulates microglial activity, and shifts the balance between neurotoxic and neuroprotective metabolites. Additionally, psychedelics affect critical signaling pathways, including the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), and mechanistic target of rapamycin (mTOR) pathways, promoting neuroplasticity and exerting anti-inflammatory effects. Beyond the serotonergic system, other neurotransmitter systems—including the glutamatergic, dopaminergic, noradrenergic, gamma-aminobutyric acid (GABAergic), and cholinergic systems—also play significant roles in mediating the effects of psychedelics. This review examines the intricate mechanisms by which psychedelics modulate neuroinflammation and underscores their potential as innovative therapeutic agents for treating neuroinflammatory and neuropsychiatric disorders.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111278"},"PeriodicalIF":5.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076381","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}
Pub Date : 2025-01-30DOI: 10.1016/j.pnpbp.2025.111277
Ming-Gang Deng , Chen Chai , Kai Wang , Zhi-Hui Zhao , Jia-Qi Nie , Fang Liu , Yuehui Liang , Jiewei Liu
Background
This study aims to investigate the genetic link between mental disorders—depression, schizophrenia (SCZ), and bipolar disorder (BIP)—and abdominal aortic aneurysm (AAA).
Methods
We first examined the genetic associations between AAA and mental disorders by analyzing global and local genetic correlations as well as shared genomic loci. Global genetic correlation was assessed using linkage disequilibrium score regression (LDSC) and the GeNetic cOVariance Analyzer (GNOVA), while local genetic correlation was analyzed using the SUPERGNOVA approach. To identify shared genetic variants, the pleiotropy-informed conditional and conjunctional false discovery rate (pleioFDR) method was applied. Subsequently, the univariate Mendelian Randomization (UMR) was employed to evaluate the causal relationship, complemented by multivariate MR (MVMR) to account for potential confounding biases. Additionally, mediation analysis was performed to determine whether known risk factors mediate the identified causal relationships.
Results
Global correlations showed positive links between depression, SCZ, and AAA, but not BIP. Local analyses identified specific genomic regions of correlation. We found 26, 141, and 10 shared loci for AAA with depression, SCZ, and BIP, respectively. UMR indicated significant associations between genetically predicted depression (OR 1.270; 95 % CI 1.071–1.504; p = 0.006) and SCZ (OR 1.047; 95 % CI 1.010–1.084; p = 0.011) with AAA, but not BIP. These results were confirmed by MVMR analyses. Mediation analyses showed that smoking, hypertension, hyperlipidemia, and coronary atherosclerosis mediated the impact of depression on AAA while smoking mediated SCZ's impact.
Conclusion
This study provides evidence that genetically predicted depression and SCZ are linked to an increased risk of AAA, mediated by traditional AAA risk factors.
{"title":"Causal relationship between mental disorders and abdominal aortic aneurysm: Insights from the genetic perspective","authors":"Ming-Gang Deng , Chen Chai , Kai Wang , Zhi-Hui Zhao , Jia-Qi Nie , Fang Liu , Yuehui Liang , Jiewei Liu","doi":"10.1016/j.pnpbp.2025.111277","DOIUrl":"10.1016/j.pnpbp.2025.111277","url":null,"abstract":"<div><h3>Background</h3><div>This study aims to investigate the genetic link between mental disorders—depression, schizophrenia (SCZ), and bipolar disorder (BIP)—and abdominal aortic aneurysm (AAA).</div></div><div><h3>Methods</h3><div>We first examined the genetic associations between AAA and mental disorders by analyzing global and local genetic correlations as well as shared genomic loci. Global genetic correlation was assessed using linkage disequilibrium score regression (LDSC) and the GeNetic cOVariance Analyzer (GNOVA), while local genetic correlation was analyzed using the SUPERGNOVA approach. To identify shared genetic variants, the pleiotropy-informed conditional and conjunctional false discovery rate (pleioFDR) method was applied. Subsequently, the univariate Mendelian Randomization (UMR) was employed to evaluate the causal relationship, complemented by multivariate MR (MVMR) to account for potential confounding biases. Additionally, mediation analysis was performed to determine whether known risk factors mediate the identified causal relationships.</div></div><div><h3>Results</h3><div>Global correlations showed positive links between depression, SCZ, and AAA, but not BIP. Local analyses identified specific genomic regions of correlation. We found 26, 141, and 10 shared loci for AAA with depression, SCZ, and BIP, respectively. UMR indicated significant associations between genetically predicted depression (OR 1.270; 95 % CI 1.071–1.504; <em>p</em> = 0.006) and SCZ (OR 1.047; 95 % CI 1.010–1.084; <em>p</em> = 0.011) with AAA, but not BIP. These results were confirmed by MVMR analyses. Mediation analyses showed that smoking, hypertension, hyperlipidemia, and coronary atherosclerosis mediated the impact of depression on AAA while smoking mediated SCZ's impact.</div></div><div><h3>Conclusion</h3><div>This study provides evidence that genetically predicted depression and SCZ are linked to an increased risk of AAA, mediated by traditional AAA risk factors.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111277"},"PeriodicalIF":5.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076371","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}
Pub Date : 2025-01-29DOI: 10.1016/j.pnpbp.2025.111271
Lei Zheng , Yinqiang Yu , Xuebing Wu , Jun Hu , Yiqun Gan
In recent decades, non-invasive brain stimulation (NIBS) has gained attention as a potential tool for promoting dietary regulation by modulating activity in the dorsolateral prefrontal cortex (dlPFC). However, the findings from individual experimental studies and meta-analyses have been inconsistent. To address this, we conducted a meta-analytic and systematic review of past studies focusing on neuromodulation of the dlPFC. Our research included 13 studies using repetitive transcranial magnetic stimulation (rTMS; 16 samples, 506 participants) and 29 transcranial direct current stimulation (tDCS; 31 samples, 1004 participants). By adjusting the pre-post correlation, we detected small-to-moderate effect sizes of NIBS on food craving (rTMS: Hedge's g = −0.57; tDCS: Hedge's g = −0.26) and food consumption (rTMS: Hedge's g = −0.51; tDCS: Hedge's g = −0.17). Additionally, we observed that the efficacy of NIBS was influenced by various moderators, including stimulation parameters, research protocols, and participant characteristics. Notably, both rTMS and tDCS appeared to enhance dlPFC function in dietary regulation for people with eating disorders or obesity. Furthermore, these effects were more pronounced with multi-session stimulation compared to single-session stimulation. Finally, based on the existing literature, we discuss the role of the dlPFC in the appetitive reward processing pathway and provide suggestions for future research directions.
{"title":"Effective non-invasive brain stimulation over dorsolateral prefrontal cortex for modulation of food craving and consumption: A systematic and meta-analytic review","authors":"Lei Zheng , Yinqiang Yu , Xuebing Wu , Jun Hu , Yiqun Gan","doi":"10.1016/j.pnpbp.2025.111271","DOIUrl":"10.1016/j.pnpbp.2025.111271","url":null,"abstract":"<div><div>In recent decades, non-invasive brain stimulation (NIBS) has gained attention as a potential tool for promoting dietary regulation by modulating activity in the dorsolateral prefrontal cortex (dlPFC). However, the findings from individual experimental studies and meta-analyses have been inconsistent. To address this, we conducted a meta-analytic and systematic review of past studies focusing on neuromodulation of the dlPFC. Our research included 13 studies using repetitive transcranial magnetic stimulation (rTMS; 16 samples, 506 participants) and 29 transcranial direct current stimulation (tDCS; 31 samples, 1004 participants). By adjusting the pre-post correlation, we detected small-to-moderate effect sizes of NIBS on food craving (rTMS: Hedge's g = −0.57; tDCS: Hedge's g = −0.26) and food consumption (rTMS: Hedge's g = −0.51; tDCS: Hedge's g = −0.17). Additionally, we observed that the efficacy of NIBS was influenced by various moderators, including stimulation parameters, research protocols, and participant characteristics. Notably, both rTMS and tDCS appeared to enhance dlPFC function in dietary regulation for people with eating disorders or obesity. Furthermore, these effects were more pronounced with multi-session stimulation compared to single-session stimulation. Finally, based on the existing literature, we discuss the role of the dlPFC in the appetitive reward processing pathway and provide suggestions for future research directions.</div></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":"137 ","pages":"Article 111271"},"PeriodicalIF":5.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076375","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}
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