FRONTIERS IN NEUROENDOCRINOLOGY神经内分泌学前沿
FRONTIERS IN NEUROENDOCRINOLOGY(英文缩写 FRONT NEUROENDOCRIN),ISSN 0091-3022,eISSN 1095-6808,中文译名:神经内分泌学前沿 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 8.333 | Q1 |
| 2022 | 7.400 | Q1 |
| 2023 | 6.500 | Q1 |
| 2024 | 6.700 | Q1 |
| 2025 | 7.000 | Q1 |
FRONTIERS IN NEUROENDOCRINOLOGY 最新收录文献
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1. Sex differences in delirium: Neuroendocrine-immune mechanisms and implications for precision neurocritical care.
PMID:日期:2026-09-07Delirium is an acute and multifactorial syndrome that remains highly prevalent in critical illness and is associated with avoidable morbidity, persistent cognitive decline, and increased mortality. Its mechanisms appear to involve a close interaction between neuroendocrine and immune pathways, including gonadal hormones, neuroactive steroids produced within the brain, and hypothalamic-pituitary-adrenal axis activity. Because these systems differ between sexes, biological sex may influence delirium risk, clinical presentation, and recovery, although this has rarely been examined in a systematic way. Here, we discuss how estradiol, progesterone, allopregnanolone, and androgens may affect microglial responses, blood-brain barrier integrity, stress reactivity, neurotransmission, inflammation, mitochondrial function, oxidative balance, and epigenetic regulation. Clinical evidence suggests possible sex-related differences in hypoactive and hyperactive presentations, antipsychotic exposure, and ICU length of stay. Future studies should integrate sex, hormonal status, neurosteroids, and cortisol dynamics to refine delirium prevention and treatment.
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2. RORA as a sex-specific molecular link in autism spectrum disorder: from transcriptional regulation to clinical phenotype across the lifespan.
PMID:日期:2026-09-03RORA is a molecular hub in autism spectrum disorder (ASD) that integrate sex steroid signaling, neurodevelopmental gene regulation, circadian rhythm, immune function and metabolic homeostasis. Convergent evidence from postmortem brain, peripheral blood, methylation profiling, animal models and cellular studies indicates that RORA is frequently downregulated in ASD, disrupting downstream pathways involved in synaptogenesis, cortical development, aromatase activity and neuroimmune balance. RORA is bidirectionally regulated by sex hormone, where androgens suppresses and estrogens activates its expression, supporting frameworks for male-biased ASD risk and the female protective effect. RORA-aromatase feedback loop further biases toward androgen dominance and reduced estrogen-mediated protection. Across the lifespan, RORA deficiency may contribute to prenatal neurodevelopmental disruption, childhood circadian and metabolic abnormalities, inflammatory dysregulation and hormone-sensitive symptom fluctuations including overlap with PMDD. Although RORA is a promising biomarker and therapeutic candidate, prospective sex-stratified longitudinal studies are required to clarify its prognostic and treatment-stratification utility in ASD.
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3. Lateral hypothalamic area: A central node for maternal behavior modulation.
PMID:日期:2026-08-31Maternal behavior emerges from neural circuits that integrate hormonal, metabolic, motivational, and sensory information. While the medial preoptic area (MPOA) is recognized as a key regulator of maternal responses, increasing evidence identifies the lateral hypothalamic area (LHA) may support successful caregiving. Through extensive connections with hypothalamic, mesolimbic, limbic, and brainstem networks, the LHA links internal physiological states to maternal behavioral output. Recent single-cell transcriptomic studies have revealed remarkable cellular and molecular diversity within the LHA, extending far beyond its traditional roles in feeding and arousal. These findings suggest that distinct LHA neuronal populations may integrate endocrine, metabolic, and social signals across pregnancy and lactation to influence maternal motivation, aggression, approach-withdrawal dynamics, and behavioral flexibility. Here, we review anatomical, functional, and transcriptomic evidence supporting a role for the LHA in maternal adaptation and propose that cell-type-specific remodeling contributes to postpartum behavioral plasticity. However, current evidence is disproportionately centered on MCH neurons, whereas the maternal functions of orexin neurons and other molecularly defined LHA populations remain largely unresolved. Moreover, whether MCH and orexin neurons exert distinct functions during early, established, and late lactation is unknown. Addressing these gaps will require temporally resolved recordings and causal manipulation of cell- and projection-defined LHA populations across postpartum stages.
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4. Dramatic sex differences leading to different brain disease presentation: The requirement for sex-specific medications with ADNP/davunetide as a case study.
PMID:日期:2026-08-10Focusing on the brain-essential gene revealed in our laboratory, activity-dependent neuroprotective protein (ADNP) and its neuroprotective site, the investigational drug davunetide (NAP), we discuss ADNP regulating steroid hormone biosynthesis and sex chromosome genes coupled with sex-dependent shuttling between the nuclei and cytoplasm. Further coupled with sex-dependent transcriptional control, ADNP/davunetide cytoplasmic microtubule/Tau targeting is translated into differential sex regulation of key cellular processes including neurogenesis, synaptic function, and axonal transport, then decoded into sexual dichotomy in multicellular processes directing sex-dependent behavioral outcomes. ADNP regulation of these sex-specific processes serves as a target for davunetide intervention, toward sex-directed precision medicine, revealing sexually dichotomized neuroprotection against tauopathy risk and progression spanning from coronary artery bypass grafting (CABG) to prodromal Alzheimer's disease, progressive supranuclear palsy (PSP), and schizophrenia, as well as the pediatric ADNP syndrome. Sex-specific intranasal bioavailability of davunetide, regulated by the estrous cycle, provides a mechanistic foundation for these differential outcomes.
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5. Freezing as a measure of fear: sex differences and implications for preclinical research.
PMID:日期:2026-08-08Rodent fear conditioning paradigms are widely used to model core features of posttraumatic stress disorder (PTSD), with freezing behaviour serving as the dominant readout. However, the extent to which freezing captures biologically and clinically relevant variability, particularly with respect to sex differences, remains unclear. We conducted a systematic review and meta-analysis of studies employing fear conditioning and extinction in wild-type rodents to assess sex differences in freezing behaviour. These were not found across studies. However, freezing levels were significantly correlated with shock intensity only in male rodents. We conclude that freezing may represent a constrained and potentially low-resolution behavioural output, which may fail to detect meaningful variation in fear processing. Given that PTSD exhibits pronounced sex differences in humans, the translational validity of commonly used behavioural endpoints may be questionable. Including both sexes and refining behavioural readouts in animal models are critical for improving the translational pipeline of stress research.
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6. The Subfornical organ: A central target for renin-angiotensin system regulation.
PMID:日期:2026-07-30The renin-angiotensin system (RAS) is a pivotal system for regulating blood volume, electrolyte balance, and systemic vascular resistance. The system exerts its functions through various central targets, particularly those located in the brain. Among these, the subfornical organ (SFO) plays a unique and integrative role. High permeability and the lack of a functional blood-brain barrier (BBB) enable the organ to monitor changes in body fluid composition and transduce these signals into autonomic and behavioral outputs. Its extensive neural projections facilitate the monitoring of circulating factors. The interaction between the RAS and the SFO has gained great attention regarding the activation of different receptors, including angiotensin AT1 and AT2 receptors, and molecular pathways such as protein kinase C, mitogen-activated protein kinase, and growth factor receptor pathways. These interactions are involved in disorders including hypertension and chronic kidney disease. This review summarizes current evidence on RAS-SFO interactions and their pathological significance.
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7. Steroid 5α-reductases in the brain: From neurosteroidogenesis to therapeutic implications.
PMID:日期:2026-07-23Steroid 5α-reductases (5αRs) catalyze the irreversible, NADPH-dependent reduction of Δ-3-ketosteroids. This process regulates major steroid signaling pathways, including neurosteroid biosynthesis, androgen activation, and glucocorticoid metabolism. By governing these processes, 5αRs influence GABAergic and dopaminergic neurotransmission, and behavioral responses to stress and reward. Although the two principal isoenzymes, 5αR1 and 5αR2, have overlapping functions, they are increasingly recognized as functionally distinct. 5αR1 supports constitutive neurosteroid synthesis in several brain regions. Conversely, 5αR2, long known for converting testosterone to dihydrotestosterone during male sexual differentiation, has emerged as the enzyme that mediates rapid allopregnanolone production in the prefrontal cortex of males during acute stress. These advances may provide a framework for understanding the complex neurobehavioral profile of 5αR inhibitors such as finasteride and dutasteride. These drugs have been associated with depression, anxiety, suicidality, sexual dysfunction, and, in some individuals, persistent sexual, somatic, and neuropsychiatric symptoms after discontinuation. At the same time, 5αR inhibition may have therapeutic value in conditions characterized by excessive or maladaptive neurosteroid signaling, including tic disorders, impulse-control disorders, and substance use disorders. In this comprehensive review, we synthesize pharmacological, genetic, and behavioral evidence on the distinct contributions of 5αR1 and 5αR2 to steroid signaling across stress, sex, and development. Finally, we outline several open questions in the biology of 5αRs, the resolution of which will be essential to advancing toward mechanistically precise and clinically actionable interventions.
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8. Light, melanin, and the microbial clock: Rewiring the gut-brain-skin axis.
PMID:日期:2026-07-01Sunlight exposure has shaped the evolutionary biology of most life forms through circadian entrainment. Full-spectrum sunlight regulates circadian rhythms, modulates gut and skin microbiomes, influences the gut-brain-skin axis, and drives dermal melanin and vitamin D synthesis. The skin acts as the body's largest photoreceptive organ and neuroendocrine hub. Melanocytes, keratinocytes, and immune cells in the skin translate photons into hormonal, metabolic, and neuronal signals. Melanin, present across vertebrate tissues, bacteria, and fungi, is a unifying photoreceptive molecule whose redox properties and signaling within the melanocortin pathway bridge host and microbial photic cues. Light signals the suprachiasmatic nucleus, triggering hypothalamic-pituitary-adrenal glucocorticoid release and peripheral clock expression throughout the gut-brain-skin axis, influencing rhythmic gastrointestinal functions, short-chain fatty acid production, and vagal feedback to the brain. Microbial photoreceptors, including melanin, flavins, and cryptochromes, extend the photoneuroendocrinology into the holobiont, revealing a shared molecular pathway through which light calibrates the host-microbe interactions. Shift work, nocturnal blue light, sun avoidance, abnormal feeding times, and circadian desynchrony disrupt the gut-brain-skin axis, resulting in dysbiosis, intestinal and skin epithelial barrier dysfunction, shifts in immune signaling, and metabolic disorders. Vitamin D intersects with these pathways, yet its possible circadian regulation remains unknown. This review synthesizes evidence positioning host and microbial melanin as the key signaling molecule of the melanocortin pathway, which is inherently circadian-regulated, governing metabolic and immune homeostasis across the gut-brain-skin axis. We outline mechanistic models and research gaps, and propose that reframing melanin as a holobiont photoreceptor opens therapeutic opportunities across dermatology, gastroenterology, and neuroendocrinology.
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9. Neuroendocrine mechanisms of stress-induced KNDy-GnRH pulse generator suppression: Linking HPA-axis activation to female reproductive dysfunction.
9. 应激诱导的KNDy-GRH脉冲发生器抑制的神经内分泌机制：将HPA轴激活与女性生殖功能障碍联系起来PMID:日期:2026-07-01Chronic stress disrupts female reproductive function, but the central mechanisms linking stress exposure to altered gonadotropin-releasing hormone (GnRH) pulsatility remain incompletely defined. The arcuate kisspeptin/neurokinin B/dynorphin (KNDy) network is a core component of the GnRH pulse generator, yet it functions within an expanded regulatory system involving fast amino-acid neurotransmission, steroid feedback, nitric oxide signaling, glial communication, metabolic cues, and stress-responsive neuropeptides. This review synthesizes evidence showing how hypothalamic-pituitary-adrenal (HPA)-axis activation may suppress KNDy-GnRH output. Corticotropin-releasing hormone, glucocorticoids, gonadotropin-inhibitory hormone/RFamide-related peptide-3, glial inflammatory mediators, serotonergic input, and energy-sensitive neuropeptides may converge to impair GnRH pulse-generator function. We further discuss the relevance of these mechanisms to functional hypothalamic amenorrhea, stress-sensitive polycystic ovary syndrome (PCOS) phenotypes, and developmental versus adult stress exposure. Overall, stress-induced reproductive dysfunction is best understood as disrupted network-level neuroendocrine rhythm regulation.
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10. Aging-related autonomic nervous system imbalance and adrenergic regulation of immunity: Implications for inflammaging, autoimmunity, and long COVID.
PMID:日期:2026-07-01The autonomic nervous system (ANS) plays a central role in immune homeostasis by integrating sympathetic and parasympathetic signals that regulate inflammation, immune cell trafficking, and tolerance. Aging is associated with a progressive autonomic imbalance characterized by sympathetic overactivation, reduced parasympathetic tone, and impaired β-adrenergic signaling in immune cells, which together contribute to inflammaging and immune dysregulation. In this review, we discuss how aging-related alterations in adrenergic pathways affect immune cell differentiation and cytokine networks, with particular emphasis on β₂-adrenergic control of the Th17/regulatory T cell balance through cAMP-dependent mechanisms interacting with cytokine-driven STAT signaling. Chronic sympathetic stimulation and β-adrenergic desensitization weaken these regulatory constraints, favoring pro-inflammatory immune trajectories and loss of immune tolerance. Finally, we propose Long COVID as a paradigmatic condition in which pre-existing inflammaging and autonomic vulnerability are amplified by viral infection, leading to persistent inflammation, impaired immune regulation, and increased susceptibility to autoimmune manifestations.