Neurobiology of Stress最新文献

{"title":"Default mode network connectivity contributes the augment effect stress recovery by natural viewing","authors":"Zini Chen ,&nbsp;Chanyu Wang ,&nbsp;Timothea Toulopoulou ,&nbsp;Xiayan Chen ,&nbsp;Lijing Niu ,&nbsp;Haowei Dai ,&nbsp;Qingzi Zhu ,&nbsp;Yuanyuan Zeng ,&nbsp;Ruibin Zhang","doi":"10.1016/j.ynstr.2025.100759","DOIUrl":"10.1016/j.ynstr.2025.100759","url":null,"abstract":"<div><div>The psychological benefits of exposure to natural environments are well established. However, whether simply viewing nature images produce similar restorative effects and the brain mechanisms involved remain unclear. For study purposes, we recruited 131 healthy university students and randomly assigned them to a nature image viewing group (NG) or a city image viewing group (CG), with 49 participants further selected (NG = 26, CG = 23) to undergo functional magnetic resonance imaging while performing behavioral tasks. First, we compared changes in subjective ratings and salivary cortisol levels, related to affect and stress between the NG and CG after stress induction and image viewing. Next, we examined differences in functional connectivity (FC) patterns of the default mode network (DMN) between the groups during image viewing. Finally, we explored correlations between the recovery effects observed after viewing nature images, along with alterations in FC. Under stress, NG participants reported greater changes in subjective ratings of positive affect (<em>t</em> = 2.610, <em>p</em> = 0.010), lower negative affect (<em>t</em> = −3.008, <em>p</em> = 0.003), and less state rumination (<em>t</em> = −2.103, <em>p</em> = 0.037). Neural data also suggest that connectivity of the DMN subsystems with attentional and executive regions plays a crucial role in modulating stress-related responses during natural experiences. Increased FC between the medial DMN subsystem and other networks was significantly correlated with behavioral recovery scores for both affect and state rumination. These findings indicate that viewing images of natural scenes can aid in stress recovery, highlighting the potential for indoor nature viewing to help mitigate psychological challenges faced in urban environments.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100759"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145100088","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":"Ventral hippocampal autophagy and mitophagy dynamics shape behavioral responses to chronic mild stress in adult male rats","authors":"Paola Brivio ,&nbsp;Maria Teresa Gallo ,&nbsp;Elena Volpari ,&nbsp;Piotr Gruca ,&nbsp;Magdalena Lason ,&nbsp;Ewa Litwa ,&nbsp;Fabio Fumagalli ,&nbsp;Mariusz Papp ,&nbsp;Francesca Calabrese","doi":"10.1016/j.ynstr.2025.100769","DOIUrl":"10.1016/j.ynstr.2025.100769","url":null,"abstract":"<div><div>Major depressive disorder (MDD) is a highly prevalent psychiatric condition characterized by a range of symptoms that often lead to reduced quality of life. Although chronic stress is a major risk factor for the development of MDD, only a subset of individuals exposed to stress develop depressive symptoms, while others remain resilient. Emerging evidence suggests that autophagy and mitophagy, key cellular processes involved in maintaining homeostasis and energy balance, may play a critical role in the response to stress. In this study, we investigated the impact of 6 weeks of chronic mild stress (CMS) on autophagy and mitophagy pathways in adult male rats, aiming to explore their potential association with vulnerability or resilience to stress-induced anhedonic-like behavior. By analyzing key autophagy and mitophagy markers in the dorsal (dHip) and ventral hippocampus (vHip), we describe region- and phenotype-specific alterations that may reflect distinct neurobiological adaptations to stress. In particular, we observed enhanced mitophagy alongside an overall impairment of autophagy in the vHip of vulnerable rats, while resilient animals showed preserved activity. These findings provide new insights into the molecular mechanisms associated with stress susceptibility and may inform future studies aimed at identifying novel therapeutic targets for MDD.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100769"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145466304","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":"Intergenerational influences of paternal combat-related trauma on offspring behavioral and brain function","authors":"Glenn R. Yamakawa ,&nbsp;James Freeman ,&nbsp;Sydney Harris ,&nbsp;Marissa Sgro ,&nbsp;Elaina Vlassopoulos ,&nbsp;Crystal N. Li ,&nbsp;Josep Roman-Juan ,&nbsp;Melanie Noel ,&nbsp;Sabrina Salberg ,&nbsp;Richelle Mychasiuk","doi":"10.1016/j.ynstr.2025.100767","DOIUrl":"10.1016/j.ynstr.2025.100767","url":null,"abstract":"<div><div>Post-traumatic stress (PTS) is a debilitating mental health condition that is highly prevalent in Veteran populations owing to their increased exposure to combat-related trauma. PTS is associated with numerous comorbid conditions including major depressive disorder, anxiety, and chronic pain. Although the causal mechanisms are currently unknown, paternal trauma has been linked to an increased risk for pathology in their offspring. Therefore, using a preclinical model of combat trauma, we examined the relationship between paternal PTS and offspring socio-emotional functioning, pain perception, and gene expression changes pertinent to HPA-axis functioning, reward processing, and epigenetic regulation. Paternally experienced trauma produced persistent changes in sire anxiety, anhedonia, and sociability, as well as elevated levels of corticosterone and changes to gene expression. In addition, the paternal experiences prior to conception changed offspring behaviour and gene expression but did not modify the offspring's stress response in adolescence. Offspring born to fathers who experienced trauma exhibited changes to nociceptive sensitivity, social and anxiety-like behaviour, as well as changes in expression of <em>5HT1A</em>, <em>5HT2A, Comt, Dnmt3a, Drd2, FKBP5, NR3C1, Maoa</em>, and <em>Mecp2</em> in the adrenal gland, hippocampus, hypothalamus, prefrontal cortex, and thalamus. These results suggest that trauma in fathers may alter expression of genes that contribute to an increased risk for the development of mental health conditions, such as PTS and chronic pain, in their offspring. This model of paternally induced intergenerational transmission could be used to explore the efficacy of future therapeutic strategies to ameliorate some risk imparted upon offspring by Veteran fathers living with PTS.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100767"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145417217","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":"Metabolic state shapes cortisol reactivity to acute stress: A systematic review and meta-analysis of metabolic and hormonal modulators","authors":"Madeleine Kördel ,&nbsp;Maria Meier ,&nbsp;Anne Kühnel ,&nbsp;Nils B. Kroemer","doi":"10.1016/j.ynstr.2025.100764","DOIUrl":"10.1016/j.ynstr.2025.100764","url":null,"abstract":"<div><div>Individual variability in cortisol stress responses is shaped by multiple physiological factors. Yet the interaction with metabolic and hormonal states remains poorly understood. Therefore, we conducted a systematic review and meta-analysis to examine how metabolic factors (particularly glucose) and sex hormone levels (progesterone and estradiol) influence cortisol reactivity to acute stress. We identified 21 studies (<em>N</em> = 1216 participants) and conducted random-effects meta-analyses for metabolic and hormonal states. Across studies, glucose administration was associated with a significant increase in cortisol responses to acute stress compared to fasting or non-glucose control conditions (<em>d</em> = 0.30, 95 % CI = [0.05, 0.60], BF₁₀ = 2.42, NNT = 10.63). In contrast, the effects of sex hormones on cortisol responses were smaller and more variable, with both progesterone and estradiol showing weak and inconsistent associations. Our results highlight a robust modulatory role of metabolic state, specifically glucose availability, on HPA axis reactivity, while evidence for sex hormone effects remains inconclusive. Future research should focus on better harmonization of designs concerning sex hormones and systematically examine interactions between metabolic and hormonal states to better explain sex differences in the prevalences of metabolic and stress-related disorders.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100764"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145268687","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":"Exposure to early-life stress uncovers shared biological signatures underlying vulnerability in the habenula and insular cortex of male and female adult rats","authors":"Valentina Zonca ,&nbsp;Moira Marizzoni ,&nbsp;Samantha Saleri ,&nbsp;Monica Mazzelli ,&nbsp;Giulia Petrillo ,&nbsp;Maria Grazia Di Benedetto ,&nbsp;Floriana De Cillis ,&nbsp;Marco Andrea Riva ,&nbsp;Annamaria Cattaneo","doi":"10.1016/j.ynstr.2025.100761","DOIUrl":"10.1016/j.ynstr.2025.100761","url":null,"abstract":"<div><div>Early-life stress (ELS) is a well-known risk factor for the development of several mental disorders later in life. The effect of ELS can be twofold: resilient individuals adapt by perceiving stress as minimal, while vulnerable ones struggle to cope with it and are predisposed to the onset of psychopathology. Although it is known that different brain regions play a role in determining ELS resilience or vulnerability, the specific mechanisms remain unclear. This preclinical study examines the effects of prenatal stress (PNS) on the functional connectivity of habenula (Hb) and insular cortex (IC) and whether these alterations predispose to stress vulnerability in adulthood. PNS was associated with reduced social interaction in both male and female animals, suggesting the onset of a potentially altered behavioural phenotype. Transcriptomic analysis of vulnerable and resilient animals revealed profound PNS-induced gene expression changes in both Hb and IC, with sex-specific patterns. In vulnerable males, pathway analysis identified a shared molecular signature between Hb and IC primarily involving the activation of inflammation and collagen-related processes. In females, vulnerability was linked to downregulation of serotonin signaling, indicating an alternative pathway to stress susceptibility compared with males. Co-expression network analysis confirmed these findings, highlighting sex-dependent biological mechanisms underlying vulnerability. These results suggest that vulnerability to stress may emerge from functional interactions between Hb and IC, mediated by distinct and sex-specific pathways.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100761"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145119557","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":"High-intensity interval training improves cognitive dysfunction in chronically stressed mice through alleviating homocysteine-induced transcriptional repression of Cldn5","authors":"Zhao-Xin Sun ,&nbsp;Mao-Yang Zhou ,&nbsp;Jin-Shan Li ,&nbsp;Yun Zhao ,&nbsp;Fang Xie ,&nbsp;Xue Wang ,&nbsp;Hong Feng ,&nbsp;Zhao-Wei Sun ,&nbsp;Ling-Jia Qian","doi":"10.1016/j.ynstr.2025.100758","DOIUrl":"10.1016/j.ynstr.2025.100758","url":null,"abstract":"<div><div>Chronic stress-induced blood-brain barrier (BBB) dysfunction contributes to neurological disorders, with homocysteine (HCY) as a key risk factor. Considering pharmacotherapy limitations, non-invasive interventions like high-intensity interval training (HIIT) are promising. To determine whether HIIT improves stress-induced BBB dysfunction and cognitive impairment, we first established a chronic unpredictable mild stress (CUMS) model and assigned mice into four groups: Control (Ctrl), CUMS, HIIT, and HIIT + CUMS. Here, we found that HIIT significantly ameliorated cognitive impairment in male CUMS mice, as evidenced by reduced escape latency in morris water maze and increased memory performance in novel object recognition test. HIIT also preserved BBB integrity by ameliorating the tight junction disruption and BBB hyper-permeability in stressed mice. Subsequently, to clarify the role of HCY in the HIIT-mediated effects, we established an HHCY model and divided mice into four groups: Ctrl, HIIT, HHCY, and HIIT + HHCY. The results showed that HIIT normalized the plasma and hippocampal HCY levels by restoring the expression of related metabolic enzymes including CBS, MTHFR and MS, and alleviated HHCY-induced cognitive decline and BBB damage. Further, HIIT reversed HCY-induced Claudin-5 downregulation by inhibiting H3K27me3 enrichment at the Cldn5 (the encoding gene of Claudin-5) promoter region. In addition, HIIT restored the expression of ETS1, one of the transcriptional activators of Cldn5, to facilitate the transcription of Cldn5 gene and the stabilization of BBB. Collectively, these findings reveal that HIIT improves chronic stress-induced cognitive impairment via eliminating the disruptive effects of HHCY on the BBB integrity, offering a non-pharmacological intervention potential for stress-related cognitive deficits.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100758"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145100033","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":"Electroacupuncture attenuates anxiety caused by chronic mild stress through inhibiting NOX2-derived oxidative stress in ventral hippocampus","authors":"Tong Yin ,&nbsp;Yinxin Wang ,&nbsp;Chuan'an Zhu ,&nbsp;Yuanfang Lin ,&nbsp;Weilin Wang ,&nbsp;Jianpeng Huang ,&nbsp;Kangwen Ming ,&nbsp;Hang Lv","doi":"10.1016/j.ynstr.2025.100768","DOIUrl":"10.1016/j.ynstr.2025.100768","url":null,"abstract":"<div><div>Anxiety disorders are highly prevalent and often triggered or worsened by chronic stress, yet current pharmacological treatments have limitations. Electroacupuncture (EA), a modern adaptation of traditional acupuncture, has shown promise as an alternative therapy for anxiety, though its mechanisms remain unclear. In this study, we investigated whether EA can alleviate anxiety-like behaviors induced by chronic mild stress (CMS) in mice, focusing on the role of NOX2-mediated oxidative stress and synaptic function in the ventral hippocampus. CMS exposure led to increased anxiety-like behavior, enhanced excitatory synaptic transmission, and elevated oxidative stress specifically in the ventral CA1 (vCA1) region. EA treatment was associated with normalization of excitatory/inhibitory synaptic balance and reduction in oxidative stress markers and NOX2 expression. Furthermore, overexpression of NOX2 in vCA1 induced anxiety-like behaviors, which EA partially ameliorated. These findings suggest that EA's anxiolytic effects may involve NOX2-related oxidative stress pathways and hippocampal excitability modulation, providing mechanistic insights that warrant further investigation for potential therapeutic applications (Graphical Abstract).</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100768"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145466303","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":"Echoes of stress: From molecular whispers to social thunderstorms","authors":"Juan Pablo Lopez","doi":"10.1016/j.ynstr.2025.100766","DOIUrl":"10.1016/j.ynstr.2025.100766","url":null,"abstract":"<div><div>Stress is often described as a fleeting feeling, a momentary surge of tension or anxiety, but in my work as a neurobiologist, I have come to understand it as something far more enduring and complex. It is not merely a reaction to external pressure, it is a biological echo that resonates through our cells, brain circuits, and peripheral systems, ultimately shaping behavior and health. These echoes begin as molecular whispers, subtle shifts in hormonal regulation, gene expression, epigenetic marks, and synaptic plasticity, but over time, they can build into thunderstorms, manifesting as psychiatric and other stress-related disorders. My research has focused on detecting and translating these echoes into meaningful biological insight. Through this perspective article, I describe how early-life adversity, sex differences, and individual variability shape susceptibility and resilience. It highlights the promise of precision tools, from single-cell technologies to AI-driven behavioral tracking, to decode stress in motion and across systems. Through studies spanning human molecular genetics, animal models, and systems neuroscience, I envision a future of stress research that embraces biological complexity, prioritizes translational relevance, and aspires to personalize mental health care by decoding the molecular and circuit-level biology of lived experience.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100766"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145417216","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":"FKBP5/FKBP51-mediated signaling pathways in neuropsychiatric diseases: Insights for biomarker development and targeted therapies","authors":"Yinglong Liu,&nbsp;Jiahe Lian,&nbsp;Youli Fu,&nbsp;Shishan Wang,&nbsp;Yongxin Liu,&nbsp;Rui Zhang,&nbsp;Huirong Han","doi":"10.1016/j.ynstr.2025.100762","DOIUrl":"10.1016/j.ynstr.2025.100762","url":null,"abstract":"<div><div>The FK506-binding protein 5 gene encodes FKBP51, a molecular chaperone linked to the pathogenesis of neuropsychiatric diseases. Recent evidence shows that FKBP51 modulates activity of the HPA axis and GR-mediated feedback via dynamic interactions with GR, thereby influencing stress adaptation, inflammatory responses, and neuronal survival. This review systematically analyzes the mechanisms by which <em>FKBP5</em> (and its encoded FKBP51) contributes to neuropsychiatric diseases and identifies shared pathways across these conditions. We further highlight key factors mediating disease variability and susceptibility: sex-, region-, and cell type-specific expression patterns of <em>FKBP5</em>/FKBP51, their temporal dynamics, genetic variants, epigenetic regulation, and gene–environment interactions. Additionally, we propose a “biphasic stress-response model” to conceptualize the temporal dynamics of <em>FKBP5</em>/FKBP51 expression during disease progression. Finally, we explore the translational potential of targeting FKBP51 signaling, and outline pharmacological strategies to modulate chaperone-dependent protein folding and stress pathways as novel therapeutic interventions.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100762"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145100087","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":"Potential vulnerability and resilience to accelerated brain aging in women exposed to stressful life events: insights from the brain age prediction model","authors":"Hyeonseok Jeong ,&nbsp;Yoonji Joo ,&nbsp;Youngeun Shim ,&nbsp;Yejin Kim ,&nbsp;Hyeonji Lee ,&nbsp;Yunjung Jin ,&nbsp;Seog Ju Kim ,&nbsp;Sujung Yoon ,&nbsp;In Kyoon Lyoo","doi":"10.1016/j.ynstr.2025.100763","DOIUrl":"10.1016/j.ynstr.2025.100763","url":null,"abstract":"<div><div>Brain age prediction models consistently reveal accelerated brain aging in psychiatric disorders, yet associations with stress, independent of formal psychiatric diagnoses, remain uncertain. This study investigated the relationships of emotional and alcohol-use symptoms, common and often comorbid stress-related symptoms, and resilience with brain aging using high-resolution structural MRI data from 520 women who experienced stressful life events. Participants were divided into four groups based on the presence of emotional and alcohol-use symptoms: no symptoms (n = 287), emotional symptoms only (n = 93), alcohol-use symptoms only (n = 79), or both symptoms (n = 61). Individual brain age gap (BAG)—the difference between predicted brain age and chronological age—was calculated using a deep learning-based brain age prediction model. Individual and interactive associations of the presence of two symptoms with BAG were assessed using two-way ANCOVA. Relationships of a continuous composite symptom score integrating both symptoms and resilience with BAG were evaluated. Participants with both symptoms exhibited significantly larger BAG than the other groups, with a statistically significant interaction between two symptom domains (p = 0.017). Across the full sample, composite symptom scores were positively associated with BAG (β = 0.16, p = 0.004), with an even stronger association within individuals with both symptoms (β = 0.34, p &lt; 0.001). Conversely, higher resilience was linked to smaller BAG across all participants (β = −0.10, p = 0.046). The negative association between resilience and BAG was statistically mediated by the composite symptom score (b = −0.011, p = 0.010). These findings may suggest a synergistic, more-than-additive association between stress-related symptoms and accelerated brain aging, as well as a potentially buffering association of resilience.</div></div>","PeriodicalId":19125,"journal":{"name":"Neurobiology of Stress","volume":"39 ","pages":"Article 100763"},"PeriodicalIF":3.6,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145156205","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}