Neuroendocrinology最新文献

{"title":"Retraction Statement.","authors":"","doi":"10.1159/000550814","DOIUrl":"10.1159/000550814","url":null,"abstract":"<p><p>The authors' accepted manuscript \"Soyasaponin Aa Prevents Obesity-Related Precocious Puberty by Inhibiting Hypothalamic-Pituitary-Gonadal Axis in Female Sprague-Dawley Rats\" [Neuroendocrinology. 2025; https://doi.org/10.1159/000550176] by Yunfei Jiang, Wen Xie, Dani Qin, Qiuju Zheng, Huiping Shen, and Yong Lei has been retracted by the Publisher and the Editor.After peer review, the accepted, unedited manuscript was published online as Early View. Before the final Version of Record was published, concerns were identified in the data underlying the study. The authors were asked to comment on the concerns. Review of the concerns and the authors' response resulted in the Editor's decision to rescind the original, provisional acceptance decision and reject the manuscript. Consequently, the published author's accepted manuscript has been retracted.The authors have been informed of this decision.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"175-176"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434359","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":"Association of Glymphatic Dysfunction with Cognitive Performance in Type 2 Diabetes Mellitus and Prediabetes.","authors":"Liya Gong, Jing He, Ziqi Wu, Mingxuan Gao, Yanmei Zeng, Wei Cui, Jingwen Luo, Junyan Wen, Ge Wen","doi":"10.1159/000551127","DOIUrl":"10.1159/000551127","url":null,"abstract":"<p><p><p>Introduction: The glymphatic system (GS) is a brain-wide clearance pathway whose dysfunction has been implicated in cognitive decline. This study was designed to assess GS alterations in prediabetes and type 2 diabetes mellitus (T2DM) using multiple MRI-derived metrics and to examine their associations with cognitive performance.</p><p><strong>Methods: </strong>This cross-sectional study was conducted from October 2023 to June 2024 at Nanfang Hospital, a tertiary care center. A total of 147 participants were recruited, including 52 patients with T2DM, 44 with prediabetes, and 51 healthy controls (HC). All participants underwent brain MRI, laboratory examinations, and cognitive function assessments. GS function was evaluated using MRI-derived metrics, including choroid plexus (CP) volume, perivascular space (PVS) volume, free water (FW) index, and the diffusion tensor imaging analysis along the PVS (DTI-ALPS) index. Group differences were tested with general linear models adjusted for sex, age, and education, and associations with clinical variables were evaluated using partial correlations.</p><p><strong>Results: </strong>Compared with HC, prediabetes showed increased CP volume and FW index, without significant changes in DTI-ALPS index or PVS volume. T2DM showed reduced DTI-ALPS index, increased CP volume, and higher FW index, with unchanged PVS volume. In both groups, lower DTI-ALPS index and higher CP volume or FW index correlated with poorer cognitive performance.</p><p><strong>Conclusion: </strong>Prediabetes and T2DM exhibit GS alterations, including reduced DTI-ALPS index and increased CP volume and FW index, which are associated with poorer cognition. GS metrics may serve as potential neuroimaging biomarkers for cognitive impairment in this population. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"189-199"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147366004","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":"A Novel Relationship between Corticotropin-Releasing Hormone Level and High-Altitude Hypoxia in Human and Rat Model.","authors":"Fan Ping Kong, Gang Xu, Ping Ping Wang, Shao Jun Chen, Ke Hao, Jian Chen, Jun Lin, Jian Wang, John Coote, Nicholas C Spitzer, Ji Zeng Du, Yang Zhao, Yu Qi Gao, Xue Qun Chen","doi":"10.1159/000549191","DOIUrl":"10.1159/000549191","url":null,"abstract":"<p><p><p>Background: Acute mountain sickness (AMS) strikes people who travel too quickly to high altitude, outstripping their ability to acclimatize. Individual susceptibility to AMS remains unpredictable. The aim of study was to investigate the neuroendocrine mechanisms regulation of corticotropin-releasing hormone (CRH) and associated with AMS.</p><p><strong>Methods: </strong>Volunteers performed exercise by cycling or by running, and the other was assigned to ascend from low to high altitude. CRH and cortisol levels were tested. AMS questionnaires were answered by volunteers. Rats were exposed in a hypobaric chamber for altitude hypoxia. CRH, Crhr1mRNA, and corticosterone levels were measured. LDH and O₂ saturation were evaluated.</p><p><strong>Results: </strong>In rats, hypobaric hypoxia resulted in increased CRH release and mRNA expression in the paraventricular nucleus (PVN). Hypobaric hypoxia also upregulated Crhr1mRNA in the pituitary and PVN in a hypoxia exposure-dependent manner, along with activation of apoptotic gene mRNA and neuronal apoptosis in cortex. These effects were associated with activation of CRHR1. Hypoxia-enhanced plasma CRH levels were negatively correlated with brain CRH level but positively with plasma corticosterone in rats. In humans, exercise at low altitude increased CRH and cortisol levels in both plasma and saliva. The increased levels in plasma correlated with increased salivary CRH. Significantly, lowlanders with high plasma CRH at low altitude developed AMS after rapid ascent to the Tibet plateau. At high altitude, lowlanders with high AMS scores had high salivary and plasma CRH levels.</p><p><strong>Conclusions: </strong>Hypobaric hypoxia is associated with high plasma CRH in rats. In humans, strong activation of CRH and CRHR1 is positively linked to AMS. CRH levels in saliva or plasma appear to predict individual responses to hypoxia. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"97-114"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12707918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145422306","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":"Multicenter Retrospective Study of Efficacy of Systemic Therapy in Patients with Neuroendocrine Tumor Grade 3 (JOSC-2001).","authors":"Hiroyuki Okuyama, Taro Shibuki, Naohiro Okano, Takuro Mizukami, Hiroaki Yanagimoto, Mao Okada, Emiri Kita, Noritoshi Kobayashi, Satoshi Kobayashi, Takaaki Furukawa, Hiroyuki Asama, Hidetaka Tsumura, Ken Kamata, Kumiko Umemoto, Yasuo Hamamoto, Yuko Suzuki, Shigeru Horiguchi, Atsushi Naganuma, Akinori Asagi, Kunihiro Tsuji, Ryoji Takada, Kazuhito Kawata, Motohiro Kojima, Hiroshi Imaoka, Takeshi Terashima, Masato Ozaka, Makoto Ueno, Masafumi Ikeda","doi":"10.1159/000548614","DOIUrl":"10.1159/000548614","url":null,"abstract":"<p><strong>Background: </strong>Neuroendocrine tumor G3 (NET G3) is a new category introduced in the WHO 2017 classification. Accordingly, evidence regarding chemotherapy for NET G3 is limited. A multicenter, retrospective analysis was performed to evaluate the outcomes of systemic therapy for NET G3 and to identify the optimal regimens.</p><p><strong>Methods: </strong>Patient demographic and treatment outcome data were retrospectively collected for 73 patients with pathologically diagnosed NET G3 who started chemotherapy at participating institutions between January 2011 and December 2019, excluding those who were ineligible by central pathological review. The chemotherapy regimens used and their efficacies were evaluated.</p><p><strong>Results: </strong>Of the 73 patients, 47 had pancreatic NETs, 10 had gastrointestinal NETs, and 16 had NETs at other sites. Central pathological review was performed for 44 patients, with a concordance rate of 95%. Initial treatment regimens included NET-based treatment (somatostatin analog, molecular-targeted agent, cytotoxic chemotherapy such as streptozocin and temozolomide) for 37 patients, neuroendocrine carcinoma (NEC)-based treatment (platinum-containing chemotherapy) for 32 patients, and other regimens for 2 patients. There were no significant differences in progression-free survival (PFS) or overall survival (OS) between patients receiving NET-based and NEC-based treatment or among the individual treatment regimens. However, the response rate (RR) was higher for NET-based cytotoxic chemotherapy (50%) compared with NEC-based treatment (16%), suggesting greater efficacy of NET-based cytotoxic chemotherapy.</p><p><strong>Conclusions: </strong>Although no significant difference in PFS or OS was found among the chemotherapy regimens for NET G3, RR was notably higher for NET-based cytotoxic chemotherapy than for NEC-based treatment.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"32-42"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145177065","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":"Direct Intra-Accumbens 17 Beta-Estradiol Administration Increases Voluntary Wheel Running in Ovariectomized Rats.","authors":"Dusti Shay, Yonca Cam, Kayla Burkle, Samantha Marquis, Brett Froeliger, Matthew J Will, Victoria J Vieira-Potter","doi":"10.1159/000550361","DOIUrl":"10.1159/000550361","url":null,"abstract":"<p><strong>Introduction: </strong>Metabolic dysfunction and the associated diseases (e.g., diabetes) are globally on the rise, and a sedentary lifestyle directly contributes to this issue. In fact, postmenopausal women are at increased risk for obesity and metabolic disease due to the loss of metabolically protective 17β-estradiol (E2). Exercise is vital for overall health, greatly reducing disease risk, but the central brain regions involved in drive for physical activity remain unclear.</p><p><strong>Methods: </strong>Female Sprague-Dawley rats were ovariectomized (OVX) and concurrently bilaterally implanted with cannulae targeting the nucleus accumbens brain region, traditionally associated with reward and addiction. Daily voluntary wheel running (VWR) was tracked before and after OVX. One month after surgery, rats were treated with intra-accumbens microinjections (0.5 μL total volume) of one of three doses of E2: 0.6 μg/μL (low), 1.5 μg/μL (moderate), or 10 μg/μL (high).</p><p><strong>Results: </strong>Daily VWR was significantly increased by intra-accumbens E2 microinjections in a non-rapid manner that persisted 48 h following microinjections.</p><p><strong>Conclusion: </strong>Findings demonstrate for the first time that intra-accumbens E2 partially rescues OVX-induced decreases in daily wheel running.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"139-150"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13069523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145948983","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":"Stress as a Neuroendocrine Modulator of the Reproductive Axis: Roles of Glucocorticoids, Kisspeptin, and Serotonergic Signalling in Animal Models.","authors":"Chawaka Osteen Chisupa, Stephen Malunga Manchishi","doi":"10.1159/000553326","DOIUrl":"10.1159/000553326","url":null,"abstract":"<p><strong>Background: </strong>Reproductive dysfunction is a major health concern affecting men and women globally, mediated by the activation of the hypothalamic-pituitary-adrenal axis as well as strongly influenced by exposure to stress. Consequently, this results in suppression of the hypothalamic-pituitary-gonadal (HPG) axis, facilitated by glucocorticoid signalling. Although we have a clear understanding of glucocorticoids as the main mediators of stress-induced reproductive suppression, evidence indicates that monoaminergic pathways, particularly serotonin (5-HT) and its receptors, play pivotal roles in linking stress to reproductive regulation. Kisspeptin neurons have emerged as crucial integrators of both glucocorticoid and serotonergic signals.</p><p><strong>Summary: </strong>Current evidence from animal studies demonstrates that stress dysregulates reproductive function at multiple levels of the HPG axis. Glucocorticoids interact through combined genomic and non-genomic pathways to suppress the secretion of kisspeptin, gonadotropin-releasing hormone (GnRH), gonadotropins, as well as gonadal steroidogenesis. In addition to the well-established glucocorticoid mechanisms, monoamines such as 5-HT play a crucial role in mediating the link between stress and reproduction. Recent molecular, electrophysiological, and transcriptomic studies have highlighted the importance of the 5-HT7 receptor, which is highly expressed in kisspeptin neurons of the arcuate nucleus (ARC), where it acts as a critical excitatory driver of GnRH/luteinising hormone (LH) pulse generation. Stress, however, suppresses serotonergic signalling by lowering 5-HT levels and suppressing serotonin receptor expression, including 5-HT7 receptor, thereby reducing kisspeptin and GnRH neuronal excitation. Glucocorticoid-mediated suppression of kisspeptin signalling might be a key underexplored pathway contributing to stress-mediated reproductive dysfunction, particularly when combined with stress-induced reductions in 5-HT and 5-HT receptor expression, suggesting a dual suppressive mechanism.</p><p><strong>Key messages: </strong>Stress suppresses reproductive function through the coordinated actions of glucocorticoids and monoaminergic, particularly serotonergic, signalling. Kisspeptin neurons situated in the ARC of the hypothalamus act as crucial integrators of glucocorticoid and serotonergic inputs and are particularly susceptible to stress-induced alterations. Normally, serotonin-mediated excitation via the 5-HT7 receptors plays an important role in promoting both kisspeptin and GnRH secretion, which are indispensable for reproductive function. However, stress downregulates 5-HT7 receptor expression in the kisspeptin-producing neurons in the arcuate, leading to the subsequent suppression of GnRH and LH pulsatility. This disruption ultimately results in reproductive dysfunction.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"439-460"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352774","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":"The Clinician's Role in Diagnostic Pathways and the Impact of Clinicopathological Collaboration on Outcomes in Patients with Neuroendocrine Neoplasms: Current Perspectives.","authors":"Alice Laffi, Andrea Lania, Alessandro Zerbi, Elisabetta Lavezzi, Silvia Carrara, Silvia Uccella","doi":"10.1159/000548924","DOIUrl":"10.1159/000548924","url":null,"abstract":"<p><strong>Introduction: </strong>Neuroendocrine neoplasms (NENs) classification and diagnosis have substantially advanced, prompting specialization of pathologists and clinicians in NEN fields and fostering close interdisciplinary collaboration. In these rare diseases, misdiagnosis may undermine therapeutic strategies, highlighting the importance of a strong clinician-pathologist partnership. While the NEN-dedicated pathologist's role is well acknowledged, in clinical practice, accurate histological review depends on the clinician's ability to pose focused diagnostic questions within a well-defined clinical context.</p><p><strong>Methods: </strong>We retrospectively analyzed all NEN histological second opinions performed by a dedicated pathologist at our ENETS Center of Excellence in 01/2023-12/2024. Second opinions were requested by referring clinicians in cases of diagnostic uncertainty or clinical-pathological discordance. Discrepancies between initial and final diagnoses were categorized as \"major\" (with a substantial impact on patients' management) or \"minor.\"</p><p><strong>Results: </strong>Of 63 reviewed cases, we identified 36 not concordant cases. Among them, we reported 29/36 (81%) cases with significant discrepancies between the initial and the final diagnosis, with a following change in therapeutic strategy in 28 (e.g., shift from surveillance to surgery or modification of systemic therapy). Clinical requests for a histological review were prompted by inconsistency between clinical history and pathological diagnosis, incomplete or incoherent initial pathology report, or need for diagnostic confirmation to support specific clinical indications (e.g., surgery or chemotherapy).</p><p><strong>Conclusion: </strong>Our findings underscore the critical role of clinician's expertise in the multidisciplinary management of NEN patients. Underestimating clinician's role in coordinating the diagnostic process can lead to suboptimal care. Additionally, there is an urgent need to redesign the NEN care pathway, ensuring early access to specialized evaluation since the early diagnostic phase.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"55-61"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145280920","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":"A Systematic Review of the Effects of N-Methyl-D-Aspartate Receptor Antagonists on Pancreatic Islets.","authors":"Sabrina Wong, Gia Han Le, John Uhlig, Ellen Yang, Christine E Dri, Joshua D Rosenblat, Rodrigo B Mansur, Roger S McIntyre","doi":"10.1159/000549276","DOIUrl":"10.1159/000549276","url":null,"abstract":"<p><p><p>Background: N-methyl-D-aspartate receptors (NMDARs) are widely distributed in the brain and pancreas. Preliminary evidence indicates that aberrant NMDAR-mediated glutamatergic signaling may disrupt pancreatic islet function and glucose-insulin homeostasis. The frequent comorbidity of depression and diabetes underscores the potential role of NMDAR signaling in pancreatic function as a shared pathophysiological mechanism. Herein, this systematic review aims to evaluate the effects of NMDAR antagonism on pancreatic cells (i.e., alpha, beta, delta) viability and function (i.e., activation, hormone production, and release).</p><p><strong>Methods: </strong>We performed a systematic search on PubMed and Ovid databases from inception to September 11, 2024. A manual search was also conducted on Google Scholar and Scopus databases. Eligible studies were primary, controlled in vitro or in vivo studies investigating the effects of NMDAR antagonism on pancreatic islet function and viability. Results were synthesized and presented descriptively. Risk of bias was assessed independently by two reviewers using a modified SYRCLE risk of bias tool.</p><p><strong>Results: </strong>We reviewed 14 studies evaluating NMDA receptor antagonism in whole islets, beta and alpha cells; however, no studies evaluated delta cells. Within beta cells, NMDAR antagonism improved glucose-stimulated insulin secretion and increased cell proliferation and viability. Similarly, alpha cells were protected against stress-induced apoptosis.</p><p><strong>Conclusion: </strong>Our results suggest that NMDAR antagonism improves alpha and beta cell function and viability, which may have translational relevance to comorbid metabolic dysfunction in depression. These mechanisms may subserve the antidepressant effects of select NMDA antagonists (e.g., ketamine/esketamine, dextromethorphan). Further research should aim to investigate the effects of subanesthetic doses of ketamine/esketamine on pancreatic function and on delta cells. </p>.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"70-87"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12734414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145409791","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":"Crosstalk between Circadian Rhythm and Neuroinflammation.","authors":"Guocheng Mei, Huiqiong Pan, Jinyu Zheng, Kepei Chen, Weihong Zheng, Hang Xu, Zhiming Liu, Wei Lin, Zhenlang Lin, Min Zhang","doi":"10.1159/000551312","DOIUrl":"10.1159/000551312","url":null,"abstract":"<p><strong>Background: </strong>The circadian rhythm is an intrinsic, approximately 24-h cycle of physiological, behavioral, and psychological changes formed through organisms' long-term evolutionary adaptation to the 24-h light-dark cycle on Earth. It regulates the body's homeostatic processes according to a daily schedule, ensuring the proper execution of physiological processes and the stability of the internal environment. In recent years, numerous studies have indicated crosstalk between the circadian rhythm and neuroinflammation. Disruption of the circadian rhythm can influence the onset and progression of various acute and chronic central nervous system diseases.</p><p><strong>Summary: </strong>This review outlines the basic components and mechanisms of the circadian timing system and divides the development of neuroinflammation into several parts: initiation of neuroinflammation, glial cell activation, disruption of the neurovascular unit, oxidative stress response, and cellular energy metabolism. By revealing the role of circadian mechanisms in each part, the relationship between the biological clock and neuroinflammation is analyzed from a molecular biology perspective, aiming to provide a new theoretical basis for the clinical intervention of neuroinflammation and the treatment of related diseases.</p><p><strong>Key messages: </strong>Disrupted circadian rhythms participate in various stages of neuroinflammation through \"crosstalk,\" making them a factor that cannot be ignored in the treatment of neurological disorders.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"229-243"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147344792","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":"Anxiety, Depression and Quality of Life in Neuroendocrine Neoplasm Patients: Insights from Regression and Network Analysis.","authors":"Kuan Zhao, Yun Liang, Jie Chen, Wei Feng","doi":"10.1159/000551891","DOIUrl":"10.1159/000551891","url":null,"abstract":"<p><strong>Background: </strong>Neuroendocrine neoplasms (NENs) are rare, heterogeneous malignancies with increasing incidence and poor survival in China. Beyond physical symptoms, patients frequently experience psychological distress and impaired quality of life (QOL), yet comprehensive evidence remains limited.</p><p><strong>Methods: </strong>Patients with NENs were recruited from the oncology outpatient clinic at Fudan University Shanghai Cancer Center. Psychological status and QOL were assessed using the Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder Questionnaire-7 (GAD-7), and the Quality-of-Life Questionnaire-Gastrointestinal Neuroendocrine Tumors-21 (QLQ-GI.NET21). Multivariable regression and network analysis were performed.</p><p><strong>Results: </strong>Among 327 patients, 34.3% exhibited significant depressive symptoms and 34.9% anxiety. Nonmetastatic NEN patients showed higher anxiety, although this finding should be interpreted with caution. Survival time, gender, tumor site, and disease phase significantly influenced anxiety and depression scores. In the gastrointestinal subgroup, G3-grade patients experienced greater distress and poorer QOL. Network analysis revealed a complex interrelationship among anxiety, depression, and QOL dimensions. High-centrality nodes included GAD2 (\"uncontrollable worry\"), the QLQ-GI.NET21 social function domain, GAD5 (\"restlessness\"), PHQ9 (\"suicide\"), and PHQ4 (\"fatigue\"). Key bridge symptoms were identified as PHQ2 (\"sad mood\"), GAD5 (\"restlessness\"), the QLQ-GI.NET21 sexual function domain, PHQ1 (\"anhedonia\"), and GAD7 (\"feeling afraid\"). Gender and metastatic status did not significantly affect network structure.</p><p><strong>Conclusion: </strong>These findings underscore the need for integrated psychological assessments and tailored interventions throughout treatment, particularly for high-risk subgroups. The core symptoms and bridge nodes identified may serve as potential targets for reducing psychological distress in NEN patients.</p>","PeriodicalId":19117,"journal":{"name":"Neuroendocrinology","volume":" ","pages":"261-274"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645873","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}