Pub Date : 2025-08-23DOI: 10.1016/j.yfrne.2025.101216
Michel Salzet
The diffuse neuroendocrine system (DNES) consists of dispersed neuroendocrine (NE) cells that bridge nervous, immune, and endocrine pathways across organs. Evolutionarily, DNES traces to primitive metazoans where single cells combined neural and immune roles, later diversifying into specialized vertebrate NE cells. Hallmark traits include dense-core granules, amine metabolism, “salt-and-pepper” chromatin, and regulation by ASCL1, NEUROG3, and INSM1. Remarkable plasticity allows immune and epithelial cells to acquire NE features under stress, while carcinomas exploit this program to form aggressive neuroendocrine tumors (NETs) and resist therapy. Canonical neuroimmune circuits, the Vagus-driven inflammatory reflex and hypothalamic–pituitary–adrenal stress axis, illustrate DNES coordination of systemic responses. Clinically, DNES-derived neoplasms span multiple organs, produce diverse hormonal syndromes, and are managed with somatostatin analogues, epigenetic drugs, and emerging immunotherapies. Recognizing DNES as a diffuse, integrative regulatory network clarifies mechanisms of chronic inflammation and cancer evolution and offers novel therapeutic entry points for disorders ranging from asthma to pancreatic neuroendocrine carcinomas.
{"title":"How the diffuse neuroendocrine system shapes health, homeostasis, and cancer","authors":"Michel Salzet","doi":"10.1016/j.yfrne.2025.101216","DOIUrl":"10.1016/j.yfrne.2025.101216","url":null,"abstract":"<div><div>The diffuse neuroendocrine system (DNES) consists of dispersed neuroendocrine (NE) cells that bridge nervous, immune, and endocrine pathways across organs. Evolutionarily, DNES traces to primitive metazoans where single cells combined neural and immune roles, later diversifying into specialized vertebrate NE cells. Hallmark traits include dense-core granules, amine metabolism, “salt-and-pepper” chromatin, and regulation by ASCL1, NEUROG3, and INSM1. Remarkable plasticity allows immune and epithelial cells to acquire NE features under stress, while carcinomas exploit this program to form aggressive neuroendocrine tumors (NETs) and resist therapy. Canonical neuroimmune circuits, the Vagus-driven inflammatory reflex and hypothalamic–pituitary–adrenal stress axis, illustrate DNES coordination of systemic responses. Clinically, DNES-derived neoplasms span multiple organs, produce diverse hormonal syndromes, and are managed with somatostatin analogues, epigenetic drugs, and emerging immunotherapies. Recognizing DNES as a diffuse, integrative regulatory network clarifies mechanisms of chronic inflammation and cancer evolution and offers novel therapeutic entry points for disorders ranging from asthma to pancreatic neuroendocrine carcinomas.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"79 ","pages":"Article 101216"},"PeriodicalIF":6.7,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-15DOI: 10.1016/j.yfrne.2025.101215
Justin Matheson , Danial Behzad , Christina Zakala , Thomas Hawken , Bruna Brands , Bernard Le Foll , Christine M. Wickens , Anthony C. Ruocco , Terri Rodak , Patricia Di Ciano
Acute cannabis exposure can transiently impair cognitive performance, increasing the risk of accidental injury and potentially disrupting activities of daily living. Although sex differences in responses to cannabis have been reported, no systematic review has examined whether these extend to acute cognitive effects. Our primary aim was to examine sex differences in the acute effects of cannabis (including isolated delta-9-tetrahydrocannabinol [THC]) on cognition in humans. Our secondary aim was to determine if sex differences in the acute effects of cannabis vary by cognitive domain, route of administration, or dosing paradigm. Following PRISMA guidelines, we conducted a comprehensive literature search across Embase, MEDLINE, APA PsycInfo, Cochrane Library, and Web of Science databases. Of 1,625 unique records, 169 underwent full-text screening, and 29 studies met inclusion criteria. Six of 29 articles (20.7 %), representing eight of 216 cognitive outcomes (3.7 %), found statistical evidence of sex differences in acute cognitive effects of cannabis/THC. All six found increased effects in female participants in at least one cognitive variable; one study additionally found increased effects in male participants, and one study found divergent cognitive effects in male and female participants. There were no clear patterns by cannabis dosing paradigm, route of administration, or cognitive domain. Overall, we found limited evidence that sex significantly influences the acute cognitive effects of cannabis, though methodological heterogeneity precludes any firm conclusions. Future studies should prioritize the measurement of sex-related factors, such as hormonal modulation of cannabinoid pharmacokinetics and pharmacodynamics.
急性大麻暴露可短暂损害认知能力，增加意外伤害的风险，并可能扰乱日常生活活动。虽然对大麻的反应有性别差异的报道，但没有系统的回顾检查这些是否延伸到急性认知影响。我们的主要目的是研究大麻（包括分离的德尔塔-9-四氢大麻酚[THC]）对人类认知的急性影响的性别差异。我们的第二个目的是确定大麻急性效应的性别差异是否因认知领域、给药途径或给药模式而异。按照PRISMA的指导方针，我们在Embase、MEDLINE、APA PsycInfo、Cochrane Library和Web of Science数据库中进行了全面的文献检索。在1,625个独特记录中，169个进行了全文筛选，29个研究符合纳入标准。29篇文章中的6篇（20.7%），代表216项认知结果中的8项（3.7%），发现了大麻/四氢大麻酚在急性认知效果方面存在性别差异的统计证据。所有六项研究都发现，女性参与者至少在一个认知变量上的影响有所增加；一项研究还发现，男性参与者的认知效果会增加，另一项研究发现，男性和女性参与者的认知效果存在差异。大麻给药方式、给药途径或认知领域没有明确的模式。总的来说，我们发现有限的证据表明性别显著影响大麻的急性认知效应，尽管方法的异质性排除了任何确定的结论。未来的研究应优先考虑性别相关因素的测量，如激素调节大麻素的药代动力学和药效学。
{"title":"Sex differences in the acute effects of cannabis on human cognition: A systematic review","authors":"Justin Matheson , Danial Behzad , Christina Zakala , Thomas Hawken , Bruna Brands , Bernard Le Foll , Christine M. Wickens , Anthony C. Ruocco , Terri Rodak , Patricia Di Ciano","doi":"10.1016/j.yfrne.2025.101215","DOIUrl":"10.1016/j.yfrne.2025.101215","url":null,"abstract":"<div><div>Acute cannabis exposure can transiently impair cognitive performance, increasing the risk of accidental injury and potentially disrupting activities of daily living. Although sex differences in responses to cannabis have been reported, no systematic review has examined whether these extend to acute cognitive effects. Our primary aim was to examine sex differences in the acute effects of cannabis (including isolated delta-9-tetrahydrocannabinol [THC]) on cognition in humans. Our secondary aim was to determine if sex differences in the acute effects of cannabis vary by cognitive domain, route of administration, or dosing paradigm. Following PRISMA guidelines, we conducted a comprehensive literature search across Embase, MEDLINE, APA PsycInfo, Cochrane Library, and Web of Science databases. Of 1,625 unique records, 169 underwent full-text screening, and 29 studies met inclusion criteria. Six of 29 articles (20.7 %), representing eight of 216 cognitive outcomes (3.7 %), found statistical evidence of sex differences in acute cognitive effects of cannabis/THC. All six found increased effects in female participants in at least one cognitive variable; one study additionally found increased effects in male participants, and one study found divergent cognitive effects in male and female participants. There were no clear patterns by cannabis dosing paradigm, route of administration, or cognitive domain. Overall, we found limited evidence that sex significantly influences the acute cognitive effects of cannabis, though methodological heterogeneity precludes any firm conclusions. Future studies should prioritize the measurement of sex-related factors, such as hormonal modulation of cannabinoid pharmacokinetics and pharmacodynamics.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"79 ","pages":"Article 101215"},"PeriodicalIF":6.7,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.yfrne.2025.101200
Fernando Castillo Díaz, Inga D. Neumann, Virginie Rappeneau
Oxytocin (OXT) plays a significant role in regulating social behaviour across various species, making it a key focus in neuroscience. Recent research has expanded beyond the established prosocial effects of OXT to explore its complex interplay with dopamine (DA), a key regulator of both reward processing and social behaviour. DA influences these behaviours both independently and in coordination with OXT. Emerging evidence highlights how psychostimulants disrupt OXT-DA interaction, exacerbating maladaptive social behaviours. This narrative review synthesises findings from pharmacological, optogenetic, and chemogenetic studies to elucidate mechanistic insights into OXT-DA crosstalk in both healthy and drug-compromised social functioning. We examined OXT-DA interaction in non-reproductive social behaviours, such as social approach and aggression, as well as reproductive behaviours, including parental care, offspring attachment, and pair bonding, both in the presence and absence of drugs of abuse. Understanding OXT-DA interaction offers important insights into the neurobiological mechanisms underlying both healthy and pathological social functioning.
{"title":"Oxytocin and dopamine in psychostimulant-induced changes in social behaviour","authors":"Fernando Castillo Díaz, Inga D. Neumann, Virginie Rappeneau","doi":"10.1016/j.yfrne.2025.101200","DOIUrl":"10.1016/j.yfrne.2025.101200","url":null,"abstract":"<div><div>Oxytocin (OXT) plays a significant role in regulating social behaviour across various species, making it a key focus in neuroscience. Recent research has expanded beyond the established prosocial effects of OXT to explore its complex interplay with dopamine (DA), a key regulator of both reward processing and social behaviour. DA influences these behaviours both independently and in coordination with OXT. Emerging evidence highlights how psychostimulants disrupt OXT-DA interaction, exacerbating maladaptive social behaviours. This narrative review synthesises findings from pharmacological, optogenetic, and chemogenetic studies to elucidate mechanistic insights into OXT-DA crosstalk in both healthy and drug-compromised social functioning. We examined OXT-DA interaction in non-reproductive social behaviours, such as social approach and aggression, as well as reproductive behaviours, including parental care, offspring attachment, and pair bonding, both in the presence and absence of drugs of abuse. Understanding OXT-DA interaction offers important insights into the neurobiological mechanisms underlying both healthy and pathological social functioning.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"78 ","pages":"Article 101200"},"PeriodicalIF":6.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.yfrne.2025.101203
Eleni Dubé-Zinatelli , Freya Anderson , Nafissa Ismail
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder affecting 6–13% of reproductive-aged women worldwide. It is primarily characterized by ovarian dysfunction, hyperandrogenism, and metabolic disturbances. However, women with PCOS also face a heightened risk of depression, possibly due to dysregulation in endocrine and immune systems and gut microbiome disturbances. Symptoms of PCOS such as infertility, obesity, and hirsutism can also cause psychological distress and further exacerbate depression symptoms. Despite this comorbidity, mental health aspects of PCOS are often overlooked in the medical field, leading to insufficient support and negative impacts on the quality of life of PCOS patients. This review explores how distinct PCOS phenotypes influence physiological and psychological outcomes and the possible biological mechanisms involved. We also examine the effects of existing treatments on PCOS symptoms and depression. Addressing both physiological and psychological challenges is crucial for developing targeted, personalized interventions that improve outcomes for individuals diagnosed with PCOS.
{"title":"The overlooked mental health burden of polycystic ovary syndrome: neurobiological insights into PCOS-related depression","authors":"Eleni Dubé-Zinatelli , Freya Anderson , Nafissa Ismail","doi":"10.1016/j.yfrne.2025.101203","DOIUrl":"10.1016/j.yfrne.2025.101203","url":null,"abstract":"<div><div>Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder affecting 6–13% of reproductive-aged women worldwide. It is primarily characterized by ovarian dysfunction, hyperandrogenism, and metabolic disturbances. However, women with PCOS also face a heightened risk of depression, possibly due to dysregulation in endocrine and immune systems and gut microbiome disturbances. Symptoms of PCOS such as infertility, obesity, and hirsutism can also cause psychological distress and further exacerbate depression symptoms. Despite this comorbidity, mental health aspects of PCOS are often overlooked in the medical field, leading to insufficient support and negative impacts on the quality of life of PCOS patients. This review explores how distinct PCOS phenotypes influence physiological and psychological outcomes and the possible biological mechanisms involved. We also examine the effects of existing treatments on PCOS symptoms and depression. Addressing both physiological and psychological challenges is crucial for developing targeted, personalized interventions that improve outcomes for individuals diagnosed with PCOS.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"78 ","pages":"Article 101203"},"PeriodicalIF":6.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.yfrne.2025.101205
Camilla Paraciani, Robbert Havekes, Peter Meerlo, Nicole J. Gervais
Sleep disturbance affects brain health, with research in rodents showing that both hippocampal memory and synaptic plasticity are impaired following sleep deprivation (SD). However, most studies have used males, overlooking sex as a biological variable (SABV). Given estradiol’s neuroprotective role in the female hippocampus, we hypothesized that the consequences of SD on memory and synaptic plasticity are modulated by sex and/or sex hormones. This review compares SD effects in males to 1) the limited findings in sleep-deprived females, and 2) the effects of estradiol in non-sleep deprived females. The few studies conducted in females suggest that memory deficits post-SD depend on hormonal state. Estradiol in non-sleep-deprived females also modulates hippocampal mechanisms of synaptic plasticity that are impaired by SD in males. While the currently available data is limited, it does hint towards sex-specific effects of SD, and emphasizes the importance of incorporating SABV in future research.
{"title":"Sex as a biological variable (SABV) modulates the consequences of sleep disturbance on hippocampal memory and synaptic plasticity","authors":"Camilla Paraciani, Robbert Havekes, Peter Meerlo, Nicole J. Gervais","doi":"10.1016/j.yfrne.2025.101205","DOIUrl":"10.1016/j.yfrne.2025.101205","url":null,"abstract":"<div><div>Sleep disturbance affects brain health, with research in rodents showing that both hippocampal memory and synaptic plasticity are impaired following sleep deprivation (SD). However, most studies have used males, overlooking sex as a biological variable (SABV). Given estradiol’s neuroprotective role in the female hippocampus, we hypothesized that the consequences of SD on memory and synaptic plasticity are modulated by sex and/or sex hormones. This review compares SD effects in males to 1) the limited findings in sleep-deprived females, and 2) the effects of estradiol in non-sleep deprived females. The few studies conducted in females suggest that memory deficits post-SD depend on hormonal state. Estradiol in non-sleep-deprived females also modulates hippocampal mechanisms of synaptic plasticity that are impaired by SD in males. While the currently available data is limited, it does hint towards sex-specific effects of SD, and emphasizes the importance of incorporating SABV in future research.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"78 ","pages":"Article 101205"},"PeriodicalIF":6.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.yfrne.2025.101206
Michelle M. Martel , Ashley G. Eng , Urveesha Nirjar , Madeline K. Petersen , Miranda P. Ramirez , Carleigh A. Litteral , Layne E. Robinson
Developmental transdiagnostic externalizing problems—including harmful substance use, conduct issues, oppositional-defiance, and ADHD-related hyperactivity-impulsivity—have significant societal impacts, contributing to high costs in areas such as incarceration, delinquency, unemployment, and relationship challenges. These issues also exhibit notable sex differences: males tend to show higher prevalence, while females, though less affected overall, often face more severe outcomes. Despite these public health and personal costs, research on externalizing problems in females remains limited, particularly regarding the biological and hormonal factors driving these sex differences. The current paper explores how female hormonal influences across developmental stages may affect externalizing behaviors, highlighting the role ovarian hormones may play in shaping these externalizing problems. During puberty, estradiol and progesterone shifts contribute to risk-taking behaviors in females, who show distinct vulnerability patterns from males. Other important and understudied reproductive periods include puberty, pregnancy and postpartum, and perimenopause and menopause, and the menstrual cycle, overall. However, most population-level studies overlook the role of ovarian hormone fluctuations. This review advocates for the integration of hormonal phases in assessments, as hormonal shifts may exacerbate symptoms or modify treatment responses. Cycle-aligned interventions and hormone stabilization strategies could improve treatment outcomes, addressing gaps in male-focused treatment models and enhancing care for females with these disorders.
{"title":"Hormonal effects on externalizing problems in females across the lifespan","authors":"Michelle M. Martel , Ashley G. Eng , Urveesha Nirjar , Madeline K. Petersen , Miranda P. Ramirez , Carleigh A. Litteral , Layne E. Robinson","doi":"10.1016/j.yfrne.2025.101206","DOIUrl":"10.1016/j.yfrne.2025.101206","url":null,"abstract":"<div><div>Developmental transdiagnostic externalizing problems—including harmful substance use, conduct issues, oppositional-defiance, and ADHD-related hyperactivity-impulsivity—have significant societal impacts, contributing to high costs in areas such as incarceration, delinquency, unemployment, and relationship challenges. These issues also exhibit notable sex differences: males tend to show higher prevalence, while females, though less affected overall, often face more severe outcomes. Despite these public health and personal costs, research on externalizing problems in females remains limited, particularly regarding the biological and hormonal factors driving these sex differences. The current paper explores how female hormonal influences across developmental stages may affect externalizing behaviors, highlighting the role ovarian hormones may play in shaping these externalizing problems. During puberty, estradiol and progesterone shifts contribute to risk-taking behaviors in females, who show distinct vulnerability patterns from males. Other important and understudied reproductive periods include puberty, pregnancy and postpartum, and perimenopause and menopause, and the menstrual cycle, overall. However, most population-level studies overlook the role of ovarian hormone fluctuations. This review advocates for the integration of hormonal phases in assessments, as hormonal shifts may exacerbate symptoms or modify treatment responses. Cycle-aligned interventions and hormone stabilization strategies could improve treatment outcomes, addressing gaps in male-focused treatment models and enhancing care for females with these disorders.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"78 ","pages":"Article 101206"},"PeriodicalIF":6.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144722236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Multiple sclerosis (MS) is the commonest autoimmune inflammatory neurological disease presenting multifocal demyelinating lesions in the white matter of the central nervous system (CNS). Its pathogenesis involves genetic and environmental mechanisms which lead to immune cell-mediated destruction of myelin and axonal damage and glial scars in CNS. Stress adaptive response might cause MS exacerbation by triggering release of hormones and neuropeptides leading to immune dysregulation and altered cytokine production. The exact link between the stress adaptive response and MS physiopathology is not clear, although neuro-immunological studies have shown alterations in cytokines and lymphocytes in MS patients, under stress, which might have clinical significance. Dysregulation of the principal components of the stress system, i.e. the hypothalamic–pituitary–adrenal axis, the sympathetic nervous system and the dopaminergic system, have been described in MS patients. In this critical review the role of the stress adaptive response in the manifestation and exacerbation of MS is described.
{"title":"The role of the stress adaptive response in multiple sclerosis","authors":"Evangelia Zapanti , Alexandros Dermentzoglou , Paraskevi Kazakou , Konstantinos Kilindireas , George Mastorakos","doi":"10.1016/j.yfrne.2025.101204","DOIUrl":"10.1016/j.yfrne.2025.101204","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is the commonest autoimmune inflammatory neurological disease presenting multifocal demyelinating lesions in the white matter of the central nervous system (CNS). Its pathogenesis involves genetic and environmental mechanisms which lead to immune cell-mediated destruction of myelin and axonal damage and glial scars in CNS. Stress adaptive response might cause MS exacerbation by triggering release of hormones and neuropeptides leading to immune dysregulation and altered cytokine production. The exact link between the stress adaptive response and MS physiopathology is not clear, although neuro-immunological studies have shown alterations in cytokines and lymphocytes in MS patients, under stress, which might have clinical significance. Dysregulation of the principal components of the stress system, i.e. the hypothalamic–pituitary–adrenal axis, the sympathetic nervous system and the dopaminergic system, have been described in MS patients. In this critical review the role of the stress adaptive response in the manifestation and exacerbation of MS is described.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"78 ","pages":"Article 101204"},"PeriodicalIF":6.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-26DOI: 10.1016/j.yfrne.2025.101202
Silvia Elisabetta Portis Bruzzone , Victoria Frederikke S. Garre , Stinne Høgh , Vibe G. Frokjaer , Kieran J. O’Donnell , Rand S. Eid
Perinatal depression (PD) is a major public mental health problem affecting 10–20% of pregnant women. Women undergo profound biological and psychosocial adaptations during pregnancy and the postpartum period. Measures of genomic function can reveal pregnancy-associated adaptations, and may also illuminate mechanisms underlying PD, offering potential for clinically useful biomarkers. A systematic overview of functional genomic signatures of PD is currently lacking. We conducted a scoping review of the current literature on two aspects of genomic function: DNA methylation and gene expression. Literature was reviewed through May 2024. Thirty-three studies met inclusion criteria. Altered genomic function related to estrogen signaling and immune function were most consistently associated with PD. However, the reviewed studies used heterogeneous molecular profiling methods, were based on small sample sizes, largely used candidate-gene approaches, and reported mixed findings. The lack of replicated signatures underscores the need for a more comprehensive assessment of genomic function in PD.
{"title":"A scoping review of functional genomics in perinatal depression","authors":"Silvia Elisabetta Portis Bruzzone , Victoria Frederikke S. Garre , Stinne Høgh , Vibe G. Frokjaer , Kieran J. O’Donnell , Rand S. Eid","doi":"10.1016/j.yfrne.2025.101202","DOIUrl":"10.1016/j.yfrne.2025.101202","url":null,"abstract":"<div><div>Perinatal depression (PD) is a major public mental health problem affecting 10–20% of pregnant women. Women undergo profound biological and psychosocial adaptations during pregnancy and the postpartum period. Measures of genomic function can reveal pregnancy-associated adaptations, and may also illuminate mechanisms underlying PD, offering potential for clinically useful biomarkers. A systematic overview of functional genomic signatures of PD is currently lacking. We conducted a scoping review of the current literature on two aspects of genomic function: DNA methylation and gene expression. Literature was reviewed through May 2024. Thirty-three studies met inclusion criteria. Altered genomic function related to estrogen signaling and immune function were most consistently associated with PD. However, the reviewed studies used heterogeneous molecular profiling methods, were based on small sample sizes, largely used candidate-gene approaches, and reported mixed findings. The lack of replicated signatures underscores the need for a more comprehensive assessment of genomic function in PD.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"78 ","pages":"Article 101202"},"PeriodicalIF":6.5,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144501906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-04DOI: 10.1016/j.yfrne.2025.101201
J. Leigh Leasure , Catherine E. Van Doorn , Kimberly Nixon
Aging and alcohol exert marked effects on the endocrine system – in particular the hypothalamic-pituitary–gonadal (HPG) and hypothalamic–pituitary–adrenal (HPA) axes. The aging female brain represents a unique substrate for alcohol effects, given that both the HPG and HPA undergo significant changes with aging in women, making this demographic notably different from both males and younger females. Little attention has been directed at alcohol effects in this group but changing trends in women’s drinking have brought these issues to the forefront. Major gaps in our understanding of aging females include how stressors common to middle and older aged women impact alcohol consumption, and how alcohol consumption in older women impacts brain health and aging. Thus, here we review the current state of knowledge concerning the unique neuroendocrinology of aging females, their stressors and pharmacokinetic reactions to alcohol, and their interactions as causes and neurotoxic consequences of excessive alcohol drinking. We highlight the role of the neuroimmune system at the intersection of aging, alcohol and stress effects, and brain endocrine systems. We conclude that therapeutic interventions should be aimed at managing alcohol-induced neuroimmune responses and their downstream effects on vulnerable white matter. In addition, mid-life represents a window of opportunity in which to introduce strategies to limit alcohol consumption and its consequences for the aging female brain. As so little is known about how alcohol intake impacts brain health in females, let alone in aging females, we assert the need for further investigation of middle-aged and aged females in human and preclinical studies.
{"title":"Binge alcohol and the neuroendocrinology of the aging female","authors":"J. Leigh Leasure , Catherine E. Van Doorn , Kimberly Nixon","doi":"10.1016/j.yfrne.2025.101201","DOIUrl":"10.1016/j.yfrne.2025.101201","url":null,"abstract":"<div><div>Aging and alcohol exert marked effects on the endocrine system – in particular the hypothalamic-pituitary–gonadal (HPG) and hypothalamic–pituitary–adrenal (HPA) axes. The aging female brain represents a unique substrate for alcohol effects, given that both the HPG and HPA undergo significant changes with aging in women, making this demographic notably different from both males and younger females. Little attention has been directed at alcohol effects in this group but changing trends in women’s drinking have brought these issues to the forefront. Major gaps in our understanding of aging females include how stressors common to middle and older aged women impact alcohol consumption, and how alcohol consumption in older women impacts brain health and aging. Thus, here we review the current state of knowledge concerning the unique neuroendocrinology of aging females, their stressors and pharmacokinetic reactions to alcohol, and their interactions as causes and neurotoxic consequences of excessive alcohol drinking. We highlight the role of the neuroimmune system at the intersection of aging, alcohol and stress effects, and brain endocrine systems. We conclude that therapeutic interventions should be aimed at managing alcohol-induced neuroimmune responses and their downstream effects on vulnerable white matter. In addition, mid-life represents a window of opportunity in which to introduce strategies to limit alcohol consumption and its consequences for the aging female brain. As so little is known about how alcohol intake impacts brain health in females, let alone in aging females, we assert the need for further investigation of middle-aged and aged females in human and preclinical studies.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"78 ","pages":"Article 101201"},"PeriodicalIF":6.5,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144230014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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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