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(Neuroendocrinology[TA])

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Neuropeptides in Immunometabolism and Neuroinflammation: Insights from Traditional Chinese Medicine. [Review]
Neuroendocrinology. 2026 Oct 12; :1. [Online ahead of print]Wu CH, Cheng CF, … Chuang WCN
Neuropeptides are small bioactive peptides secreted by neurons and immune cells that serve as critical messengers in both central and peripheral systems. Recent studies have identified key neuropeptides-such as Substance P (SP), Vasoactive Intestinal Peptide (VIP), Neuropeptide Y (NPY), and Calcitonin Gene-Related Peptide (CGRP)-as pivotal regulators of immunometabolism and neuroinflammation. The…
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Erratum. [Published Erratum]
Neuroendocrinology. 2026 Oct 05; :1. [Online ahead of print]
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This is a correction to: Zhenwei Li, Yinzi Wu, Yike Gao, Ming Feng, Kan Deng, Bing Xing, Wei Lian, Yong Yao, Renzhi Wang, Jian Sun, Xinjie Bao; Pathological Classification and Clinical Characteristics of Growth Hormone-Secreting PitNETs. [Neuroendocrinology. 2026; https://doi.org/10.1159/000552989].In the originally published version of this article, Yike Gao was inadvertently omitted from the eq…
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Progress on Mechanisms of Therapeutic Potential of Oxygen Delivery in Brain Disorders. [Review]
Neuroendocrinology. 2026 Sep 10; :1. [Online ahead of print]Lv J, Guo DN
CONCLUSIONS: We examine the molecular machinery of oxygen sensing, including the canonical prolyl hydroxylase domain/hypoxia-inducible factor/von Hippel-Lindau (PHD-HIF-pVHL) pathway as well as newly identified oxygen sensors such as Jumonji C domain histone demethylases and 2-aminoethanethiol (cysteamine) dioxygenase. We then explore how perturbations in oxygen delivery contribute to neurodegenerative diseases, stroke, traumatic brain injury, and neurodevelopmental disorders. Emerging therapeutic strategies are critically evaluated, including normobaric and hyperbaric oxygen therapy, therapeutic acute intermittent hypoxia, hypoxia preconditioning, and pharmacological targeting of oxygen-sensing pathways.Moreover, the emerging concept of tissue-specific oxygen "set points" suggests that both hypoxia and hyperoxia can be pathological and that restoring optimal oxygenation, rather than simply maximizing oxygen delivery, may represent a more nuanced therapeutic approach. Notably, recent preclinical evidence demonstrating that hypoxia itself can reverse pathology in mitochondrial disease models challenges conventional assumptions and opens new avenues for treating brain disorders characterized by relative hyperoxia. Understanding the mechanisms by which oxygen delivery influences neuroinflammation, mitochondrial function, and neural plasticity will be essential for translating these insights into effective clinical interventions.
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Should PTCH1 be Considered as a Kallman Syndrome Gene? [Letter]
Neuroendocrinology. 2026 Sep 09; :1. [Online ahead of print]Hercent A, Tchernitchko DN
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The Thyroid-Brain Network: Exploring Inflammation, Immune Mechanisms and Common Triggers in Thyroid-Related Neurological Dysfunction. [Review]
Neuroendocrinology. 2026 Sep 08; :1. [Online ahead of print]Ullah MFN
Autoimmune thyroid diseases (AITD), including Hashimoto's thyroiditis and Graves' disease, represent the most prevalent endocrine disorders worldwide, affecting hundreds of millions with profound but often under recognized neurological consequences. There are emerging lines of evidence establishing inflammation and immunity as the critical missing link connecting peripheral thyroid dysfunction to…
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Autoimmune thyroid diseases (AITD), including Hashimoto's thyroiditis and Graves' disease, represent the most prevalent endocrine disorders worldwide, affecting hundreds of millions with profound but often under recognized neurological consequences. There are emerging lines of evidence establishing inflammation and immunity as the critical missing link connecting peripheral thyroid dysfunction to central nervous system manifestations. Thyroid hormones function as essential neuromodulators governing neurodevelopment, synaptic plasticity, and cognitive processing through integrated genomic and non-genomic mechanisms, with region-specific cerebral metabolic disturbances correlating with distinct neuropsychiatric symptoms. The immunological perspective reveals that AITD propagates neuroinflammation through convergent pathways: molecular mimicry enabling cross-reactivity between thyroid and neural antigens, cytokine-mediated disruption of neurotransmitter metabolism, HMGB1-driven glial activation, and blood-brain barrier compromise facilitating immune cell infiltration. The thyroid-gut-microbiota axis emerges as a critical mediator wherein dysbiosis perpetuates both thyroid autoimmunity and neuroinflammation through impaired serotonin precursor availability and increased intestinal permeability. Mitochondrial dysfunction represents an energetic common denominator, as thyroid hormone dysregulation directly impairs oxidative phosphorylation, producing region-specific cerebral metabolic disturbances. Simultaneous compromise of monoamine systems, cholinergic signaling abnormalities, and glutamate excitotoxicity creates a particularly toxic neurochemical state in untreated thyroid dysfunction. Common triggers such as psychological stress, gut dysbiosis, and mitochondrial impairment may activate interconnected pathways that simultaneously compromise thyroid and brain function, revealing that these disorders share fundamental mechanistic origins. These insights have been discussed in the current review to enhance the understanding of thyroid-brain function, the core mechanisms and consequences of functional deficits.

Medial Preoptic Nucleus to Periaqueductal Gray GABAergic Pathway Underlies Individual Differences in Consolation-Like Behavior in Mice. [Journal Article]
Neuroendocrinology. 2026; 116(6):392-406.Wu JW, Tian J, … Li LFN
CONCLUSIONS: The MPNGABA-PAG pathway is a critical modulator of individual variation in consolation-like behavior in mice, revealing a subregion- and cell-type-specific circuit mechanism underlying empathic heterogeneity.
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Contrast-Enhanced CT Features for Identifying Primary Origin and Differentiation Grade of Neuroendocrine Liver Metastases. [Journal Article]
Neuroendocrinology. 2026 Jul 16; :1-12. [Online ahead of print]Qu Y, Sheng L, … Qin YN
CONCLUSIONS: The hypoenhancement of NELM facilitates identification of non-pancreatic primaries, and the presence of an ill-defined margin and a targetoid appearance are indicative of NEC. These features can aid in optimizing management strategies in patients with NELM.
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Neuropsychological Outcomes and Behavioral Profiles in Children with Congenital Hypothyroidism: Impact of Timing of Thyroxine Initiation - A Cross-Sectional Study from Southern India. [Journal Article]
Neuroendocrinology. 2026 Jul 16; :1-9. [Online ahead of print]Nalluri BT, Aitha A, … Sahay RKN
CONCLUSIONS: Children with CH in this Indian cohort demonstrated substantially lower IQ compared to internationally reported values, attributable to delayed diagnosis and suboptimal therapy adherence. Males exhibited more severe biochemical disease at diagnosis and greater neurocognitive impairment. Routine behavioral assessment and cognitive behavioral therapy should be incorporated into standard CH follow-up in resource-limited settings.
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Complex Interactions between Abnormal Thyroid Function and Neurodevelopmental Disorders: A Mendelian Randomization Study. [Journal Article]
Neuroendocrinology. 2026 Jul 16; :1-13. [Online ahead of print]Li XAA, Li Z, … Ding ZN
CONCLUSIONS: Our study provides new insights into the relationship between NDDs and thyroid dysfunction. It suggests that there were potential risk factors and causal pathways and calls for early diagnosis, intervention, and integrated health care.
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Reproduction under Siege: How Chronic Stress Hijacks the HPG Axis? [Review]
Neuroendocrinology. 2026 Jul 14; :1-21. [Online ahead of print]Xu D, Zhao X, … Wang C
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CONCLUSIONS: This review synthesizes evidence that chronic stress acts on the HPG axis at multiple levels: hypothalamic-pituitary-adrenal (HPA)-derived corticotropin-releasing hormone and glucocorticoids suppress the gonadotropin-releasing hormone (GnRH) pulse generator through kisspeptin/KNDy and gonadotropin-inhibitory hormone pathways; sympathetic overdrive impairs gonadal steroidogenesis while parasympathetic tone declines; and metabolic-inflammatory crosstalk amplifies suppression. The resulting decline in sex steroids - estradiol, progesterone, and testosterone - creates sex-specific vicious cycles that further dysregulate stress and immune circuits, contributing to affective, reproductive, and neurodegenerative disorders.The HPG axis serves as a critical hub integrating stress signals, and its suppression is an active, regulated process with distinct sex differences. Hormone-based interventions, including estrogen, neurosteroid analogs, and testosterone, show therapeutic promise for stress-related conditions, and future research should focus on the neural circuits and molecular switches that govern HPA-HPG crosstalk to enable personalized, neuroendocrine-informed therapies.
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Dynamic Profiles of Serum Kisspeptin and Delta-Like 1 Homolog during Gonadotropin-Releasing Hormone Stimulation in Central Precocious Puberty and Premature Thelarche. [Journal Article]
Neuroendocrinology. 2026 Jul 09; :1-9. [Online ahead of print]Paisansukanant K, Chatdamrongsakool K, … Srilanchakon KN
CONCLUSIONS: Our findings indicate that the dynamic profiles of kisspeptin and DLK1 reflect distinct neuroendocrine mechanisms distinguishing CPP from PT. These findings underscore the complexity of neuroendocrine regulation of puberty involving kisspeptin and DLK1; however, given the considerable overlap between CPP and PT patients observed in this study, their diagnostic potential as standalone or adjunctive clinical tools remains uncertain and would require validation in larger, independent cohorts.
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The Correlation between Thyroid Function and Mental Disorders: An Overview and Future Perspectives. [Review]
Neuroendocrinology. 2026 Jul 09; :1-17. [Online ahead of print]Cheng K, Zhang Y, Zhang CN
CONCLUSIONS: This article systematically reviews the epidemiological characteristics of thyroid dysfunction, the physiological functions of THs, population heterogeneity, and patterns of comorbidity between thyroid disorders and mental disorders. It focuses on the pathological mechanisms linking thyroid function to major mental disorders including depression, anxiety, bipolar disorder, and schizophrenia. In addition, this article prospects future research directions, addresses current study limitations, and points to interdisciplinary approaches for clinical management, providing comprehensive evidence-based support for the combined screening and precision intervention of thyroid diseases and mental disorders.The paper clearly identifies the pathogenic role and biomarker value of thyroid autoantibodies, the adjunctive role of TH supplementation in the treatment of mental disorders, and the early clinical significance of thyroid function screening, further highlighting the clinical value of their interactive relationship.
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Passive Smoking and Thyroid Diseases: Association by Mendelian Randomization Study. [Journal Article]
Neuroendocrinology. 2026 Jul 02; :1-11. [Online ahead of print]Li P, Cai N, … Wang QN
CONCLUSIONS: This study provides suggestive evidence that genetically predicted passive smoking may be associated with increased risks of Graves' disease and thyroid cancer, as well as an inverse association with nontoxic single thyroid nodules. These findings support efforts to minimize exposure to tobacco smoke among passive smokers. The inverse association with nontoxic single thyroid nodules should be interpreted cautiously and warrants further investigation. Further studies using larger and more granular datasets are required to clarify the potential causal relationships between passive smoking and thyroid diseases.
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Erratum. [Published Erratum]
Neuroendocrinology. 2026; 116(5):349-352.
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In the article "Expanded Targeted-Exome Sequencing and Functional Validation Improve Molecular Diagnosis and Refine Genotype-Phenotype Correlations in Congenital Hypogonadotropic Hypogonadism" [Neuroendocrinology. 2026;116(1):1-17; https://doi.org/10.1159/000548348] by Fausto et al., the authors identified an error in the nomenclature of the protein variant associated with the genetic variant.The…
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In the article "Expanded Targeted-Exome Sequencing and Functional Validation Improve Molecular Diagnosis and Refine Genotype-Phenotype Correlations in Congenital Hypogonadotropic Hypogonadism" [Neuroendocrinology. 2026;116(1):1-17; https://doi.org/10.1159/000548348] by Fausto et al., the authors identified an error in the nomenclature of the protein variant associated with the genetic variant.The authors note that the variant affects the stop codon (Ter / *) at position 139, converting it to a Trp codon (a no-stop variant) and resulting in a C-terminal extension of the protein. Translation continues for seven amino acids beyond the original termination site before reaching a new stop codon (Ter / *) at position 7 of the added sequence. Accordingly, the protein change should be corrected from p.*139Trpext*41 to p.*139Trpext*7, following the recommendations of the Human Genome Variation Society (HGVS) protein extension nomenclature guidelines (https://hgvs-nomenclature.org/stable/recommendations/protein/extension/).The corrected Table 2 is shown here.Table 2.Novel and known pathogenic/likely pathogenic variants and VUS identified by the 52-gene CHH exome panel in our cohort of 35 patients with CHHIDFamilial historyGeneVariantTypeZygosityMAF (GnomAD/AbraOM)ACGMReference1sporadicSPRY4c.19A>Gmissensehtz<0.005/NRVUS (PM2, BP4)Novelp.Thr7Ala2sporadicIL17RDc.1705C>Tmissensehtz<0.02/NRVUS (PM2, BS2, BP1, BP4)Novel (RCV:004212115.1)p.Pro569Ser3sporadicWDR11c.1303G>Amissensehtz<0.015/NRPathogenic (PS1, PS3)[42]p.Ala435Thr4sporadicANOS1c.1369C>TnonsensehmNR/NRPathogenic (PVS1, PS1)[43]p.Arg457*5sporadicCHD7c.2978A>Tmissensehtz<0.007/NRVUS (PM1-PM2-PP3)Novelp.Asp993ValPCSK1c.239G>Amissensehtz<0.007/NRLikely pathogenic (PS1, PM2, PM5)[44]p.Arg80Gln6familialKISS1c.417delAnostop (stoploss)htz<0.001/0.206VUS (PM2, PM4)Novel (RCV: 001730690.2)p.*139Trpext*77sporadicTACR3c.1115G>Amissensehtz<0.004/NRVUS (PM2, PP2, PP5)Novelp.Arg372His8familialPROKR2c.802C>Tmissensehtz<0.01/0.009VUS (PS3)[61]p.Arg268Cys9sporadicIGSF10c.467G>Tmissensehtz<0.005/0.002VUS (PM1, PM2, PP5, BP1)Novelp.Arg156Leu10sporadicPROKR2c.868C>Tmissensehtz<0.01/NRPathogenic (PS1, PM1, PM2, PP2, PP3, PP5)[15, 45, 47]p.Pro290Ser11familialGNRHRc.806C>Tmissensehm<0.0002/NRPathogenic[21, 48]CHD7p.Thr269Metmissensehtz<0.001/NRVUS (PM2,BP4)Novel (RCV: 000819615.6)GHSRc.577A>Gmissensehtz0.003/0.0016VUS (PM2, BP4)Novel (RCV: 001149557.4)KISS1p.Met193Valmissensehtz0.01/0.006VUS (PP3)Novel (RCV: 003730668.1)MSX1c.10 72G>Amissensehtz0.001/NRVUS (PM2, PP3)Novel (RCV: 000983935.6)SEMA3Ap.Ala358Thrmissensehm0.01/0.008VUS (PP3)Novel (RCV: 002489291.1)c.268C>Tp.His90Aspc.821C>Tp.Ala274Valc.1000A>Gp.Ile334Val12familialKISS1Rc.608C>Amissensehm<0.007/NRLikely pathogenic (PS3, PM1, PM2, PP2)present studyp.Ala203Asp13sporadicANOS1c.712C>TnonsensehtzNR/NRPathogenic (PVS1, PM2, PP3)Novelp.Gln238*14sporadicOTUD4c.910G>Amissensehtz<0.003/0.0008VUS (PM2, BP4)NovelSPRY4p.Thr349Promissensehtz<0.004/NRLikely pathogenic (PS1, PM1, PM2)[35]c.824G>Ap.Val304Ile15sporadicCHD7c.2199dupduplicationhtz<0.01/NRPathogenic (PVS1, PM2, PP4)NovelTACR3p.Ser734Ilefs*5nonsensehtz<0.01/NRPathogenic (PVS1, PS1, PM2, BP4)[49, 50]c.824G>A p.Trp275*17sporadicCHD7c.3299G>Amissensehtz<0.003/0.0008VUS (PM2, PP3)Novel (RCV: 000326831.5)POLR3Ap.Arg1100Hismissensehm<0.005/NRVUS (PM2, PP3)Novel (RCV: 003020802.2)c.2444A>Tp.Asn815Ile18familialCHD7c.6989G>Cmissensehtz<0.004/NRVUS (PM2, PP2, PP3)Novel (RCV: 000880727.5)FGFR1p.Gly2330Alaintronic (loss of splice donor site)htzNR/NRPathogenic (PVS1, PM2, PP3)Novelc.1663+5G>A19sporadicSPRY4c.824G>Amissensehtz<0.004/NRLikely pathogenic (PS1, PM1, PM2)[35]p.Val304Ile20sporadicCHD7c.5738T>Cmissensehtz<0.0009/NRVUS (PM2-PP3)Novel (RCV: 002251062.1)DUSP6p.Leu1913Promissensehtz<0.005/0.002VUS (PM2-BP1)Novel (RCV: 003717071.1)c.35C>Tp.Ser12Leu21sporadicGHSRc.545T>Cmissensehtz<0.01/0.0008Likely pathogenic (PS3, PM2, PP3, PP5)NovelPLXNA1p.Val182Alamissensehtz<0.005/NRVUS (PM2-BP1)Novel (RCV: 003963777.1)c.3761G>Tp.Gly1254Val22sporadicIGSF1dup chrX: 130,411,829-130,420,648copy number gain (x2)htz<0.001Likely pathogenic (score: 0.9)Novel(8.8 Kb)23familialPROK2c.297dupduplicationhtz0.0104/NRPathogenic (PVS1, PM2, PP3)[8]p.Gly100Trpfs*2224sporadicDMXL2c.3860G>Tmissensehtz<0.052/NRVUS (PM2, PP3)Novel (RCV: 002489372.1)p.Ser1287Ile25sporadicANOS1c.318+2T>CintronichemNR/NRPathogenic (PVS1, PM2, PP3)Novel26sporadicFGFR1c.106G>deldeletionhtzNR/NRPathogenic (PVS1, PM2, PP3)NovelDMXL2p.Ala36Profs*67missensehtzNR/NRVUS (PM2, PP3, BP4)NovelDMXL2c.8624A>Gmissensehtz0.0003/NRVUS (PM2, PP3, BP4)Novel (RCV: 001957785.2)PNPLA6p.Asn2874Sermissensehtz<0.02/NRVUS (PM2, BP1)Novel (RCV: 001338478.4)c.6946T>Cp.Ser2316Proc.3598C>Gp.Gln1200Glu28sporadicCHD7c.2786dupduplicationhtzNR/NRLikely pathogenic (PVS1-PM2)NovelGHSRp.Glu930Argfs*4missensehtz<0.002/NRVUS (PM2,PP3)Novelc.505G>A p.Ala169Thr29familialFGFR1c.630T>Gnonsensehtz<0.002/NRPathogenic (PVS1, PM2, PP3)Novel (RCV: 003234647.1)IGFALSp.Tyr210*missenseNR/NRVUS (PM2, PP3)Novelc.830G>Ap.Arg277His31sporadicCHD7c.1774del: Gln592Serfs*16deletionhtz<0.003/NRPathogenic (PVS1, PM2, PM5)NovelDMXL2del Chr15: 51,785,818-51,868,914copy number loss (83.1 Kb)htzNR/Pathogenic (score: 1.15)NovelDMXL2c.5590A>Gmissensehtz<0.01/NRVUS (PM2, PP3, BP4)Novel (RCV: 002623884.1)p.Thr1864Ala 33sporadicSOX2del chr3: 180,320,049-181,431,102copy number loss (1.1 Mb)htz-Pathogenic (score:1.2)Novel34sporadicCHD7c.6275A>Gmissensehtz<0.001/NRVUS (PM2,PP3)Novelp.Glu2092Gly35sporadicSPRY4c.796G>Amissensehtz<0.001/NRVUS (PM2, PP3)Novelp.Val266MetPatients harboring any variant: 21/35 (60%); total found variants: 49 (46 SNVs and 3 CNVs); pathogenic variants: 16/49 (32.7%); likely pathogenic variants: 6/49 (12.2%); VUS: 27/49 (55.1%). NR, not reported in the GnomAD or AbraOM dataset; RCV, Reference ClinVar.

Stress as a Neuroendocrine Modulator of the Reproductive Axis: Roles of Glucocorticoids, Kisspeptin, and Serotonergic Signalling in Animal Models. [Review]
Neuroendocrinology. 2026; 116(6):439-460.Chisupa CO, Manchishi SMN
CONCLUSIONS: 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.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.
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