Brain, behavior, & immunity - health最新文献

{"title":"Corrigendum to “Animal models of Huntington's disease. Pros and cons” [Brain, Behavior, Immunity Health 50 (2025) 101149","authors":"Polina Stepanova , Ove Eriksson , Merja H. Voutilainen , Dan Lindholm","doi":"10.1016/j.bbih.2026.101180","DOIUrl":"10.1016/j.bbih.2026.101180","url":null,"abstract":"","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101180"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of health behaviors in links between stress and epigenetic aging","authors":"Marlon Goering ,&nbsp;Kyle J. Bourassa ,&nbsp;Maxine Weinstein ,&nbsp;Anthony P. Auger ,&nbsp;Casey K. Brown","doi":"10.1016/j.bbih.2026.101194","DOIUrl":"10.1016/j.bbih.2026.101194","url":null,"abstract":"<div><div>High levels of stress are associated with accelerated epigenetic aging and health risks. However, less is known about the independent effects of different types of stress and whether these effects are explained by unhealthy behaviors. This study involved 1308 adults from the Midlife in the United States (MIDUS) study (53% female; 69% White, 22% Black; mean age: 54 years) to examine the independent effects of stressful life events and perceived stress on three DNA methylation-based measures of epigenetic aging (DNAm measures: GrimAge, DunedinPACE, PhenoAge). We also tested whether tobacco use, alcohol use, sleep problems, low diet quality, and low physical exercise mediate these effects. The results indicated that both perceived stress and stressful life events independently predict accelerated epigenetic aging indirectly through unhealthy behaviors across multiple DNAm measures of aging. Specifically, perceived stress predicted accelerated epigenetic aging through more sleep problems, lower diet quality, and lower physical exercise, whereas stressful life events predicted accelerated epigenetic aging through more tobacco and alcohol use as well as sleep problems. In addition, stressful life events directly predicted accelerated GrimAge above and beyond health behaviors. In summary, these findings underscore the critical role of health behaviors in linking different types of stress with biological aging and associated health issues.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101194"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146189477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimal doses of mind-body exercise on neuroinflammation in individuals with neuropsychiatric disorders: A systematic review and dose-response meta-analysis","authors":"Qingying Zheng ,&nbsp;Guoyuan Huang ,&nbsp;Qian Liu ,&nbsp;Weiguang Ni ,&nbsp;Ying Zhao","doi":"10.1016/j.bbih.2026.101176","DOIUrl":"10.1016/j.bbih.2026.101176","url":null,"abstract":"<div><h3>Background</h3><div>Mind-body exercises (MBEs), including Tai Chi (TC), Qigong (QG), Yoga (YG), and Mindfulness-Based Stress Reduction (MBSR), show promise in neuropsychiatric rehabilitation by modulating neuroinflammation. This study systematically examines the effects of MBEs on neuroinflammation-related biomarkers in neuropsychiatric disorders, aiming to identify optimal modalities, dosages, and key moderators.</div></div><div><h3>Methods</h3><div>Databases were systematically searched for eligible RCTs from inception until February 2025. Data were analyzed using R packages (“<em>meta</em>,” “<em>multinma</em>,” “<em>MBNMAdose</em>,” “<em>GEMTC</em>,” “<em>BUGSnet</em>,” “<em>ggplot2</em>”) to assess the effects of MBEs on TNF-α, IL-6, IL-1β, IL-10, CRP, and BDNF in adults with neuropsychiatric disorders.</div></div><div><h3>Results</h3><div>Twenty-nine RCTs involving 2253 participants were included. MBEs significantly reduced IL-6 [standardized mean difference (SMD) = −0.47] and IL-1β [SMD = −0.90], while increasing BDNF [SMD = 1.08] and IL-10 [SMD = 0.87]. Effects on TNF-α [SMD = −0.33] and CRP [SMD = −0.12] showed a non-significant trend toward benefit. Dosages between 600 and 1000 MET-min/week yielded the most pronounced anti-inflammatory effects. Network meta-analysis ranked TC and MBSR as the most effective for reducing proinflammatory cytokines, while QG showed the greatest benefits for neurotrophic outcomes. Participant characteristics (age, population, clinical conditions) and MBE parameters (duration, frequency, session length) significantly moderated neuroprotective effects.</div></div><div><h3>Conclusion</h3><div>MBEs effectively reduce proinflammatory cytokines (IL-1β, IL-6) and enhance anti-inflammatory cytokine (IL-10) and neurotrophic factor (BDNF) in neuropsychiatric disorders. The optimal dosage ranges from 600 to 1000 MET-min/week. Given the impact of participant characteristics and MBE parameters, personalized prescriptions may enhance clinical outcomes and long-term neuroprotective effects.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101176"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune dysregulation and neuroinflammation in bipolar disorder: Pathophysiological insights and therapeutic perspectives","authors":"Floriana De Cillis ,&nbsp;Veronica Begni ,&nbsp;Ilari D'Aprile ,&nbsp;Giulia Petrillo ,&nbsp;Marco Andrea Riva ,&nbsp;Annamaria Cattaneo","doi":"10.1016/j.bbih.2025.101155","DOIUrl":"10.1016/j.bbih.2025.101155","url":null,"abstract":"<div><div>Bipolar disorder (BD) is increasingly associated with immune system dysregulation encompassing both peripheral and central components. Peripheral low-grade inflammation, marked by elevated proinflammatory cytokines and impaired anti-inflammatory responses, contributes to systemic immune imbalance in BD. This peripheral inflammatory state may compromise blood–brain barrier (BBB) integrity, facilitating the entry of peripheral immune mediators into the central nervous system (CNS) and triggering neuroinflammatory cascades. Within the CNS, neuroinflammation is orchestrated primarily by microglial and astrocytic activation, which disrupts neuronal homeostasis and synaptic function. Additionally, oxidative stress acts as a crucial mediator, exacerbating neuronal damage. Based on current findings, this review synthesises evidence linking both central and peripheral inflammation to the pathophysiology of BD, offering a perspective on its underlying biology. A comprehensive understanding of the dynamic interplay between peripheral inflammation and central neuroimmune responses is essential for identifying novel therapeutic targets and developing interventions that effectively address both systemic and CNS components of BD pathophysiology.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101155"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145898084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between influenza A virus and SARS-CoV-2 infections and mood disorders","authors":"Yanling Xiang ,&nbsp;Wanqi Wang ,&nbsp;Jinyi Zhu ,&nbsp;Zexing Chen ,&nbsp;Wanyi Huang","doi":"10.1016/j.bbih.2026.101182","DOIUrl":"10.1016/j.bbih.2026.101182","url":null,"abstract":"<div><div>Acute respiratory infections (ARIs) are among the most common infectious diseases encountered in clinical practice, with approximately 70–80 % of cases attributed to viral pathogens. Among these, seasonal influenza A virus (IAV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) persistently pose public health threats due to their high genetic variability, strong transmissibility and significant pathogenicity. Recently, accumulating evidence has suggested that these viruses can not only cause typical respiratory symptoms but also affect the central nervous system (CNS) through neuroinvasion and inflammation, thereby increasing the risk of developing or exacerbating mood disorders such as anxiety and depression. This makes them significant complications affecting patient prognosis and public health resources.</div><div>This comorbidity between infection and mood disorders exhibits a complex bidirectional relationship. Beyond viral CNS involvement, individuals with mood disorders appear to be more susceptible to IAV and SARS-CoV-2 infections and may be at greater risk of developing severe illness. This comorbidity not only significantly impairs quality of life and clinical outcomes but also places a substantial burden on healthcare systems and public health infrastructure.</div><div>Therefore, this review aims to summarize the clinical characteristics of IAV and SARS-CoV-2 infections comorbid with mood disorders. Based on existing evidence, we innovatively distinguish two mechanism pathways: an externally driven pathway dominated by psychological stress (acute stress), and an internal biological pathway represented by immune dysregulation and gut microbiota imbalance. This classification will provide a theoretical framework and research direction for accurately identifying acute stress responses and persistent neuropathology, as well as for future basic research and targeted intervention strategies.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101182"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endotoxin-induced inflammation promotes, via the adrenomedullary system, a hyperglycemic and anti-inflammatory reflex","authors":"Esteban Santacruz-Martínez,&nbsp;Eva Soto-Tinoco,&nbsp;Ruud M. Buijs","doi":"10.1016/j.bbih.2026.101183","DOIUrl":"10.1016/j.bbih.2026.101183","url":null,"abstract":"<div><div>Immune challenges elicit significant physiological responses which are coordinated by the central nervous system. Among these is the sympathetic system-mediated anti-inflammatory reflex, which suppresses the TNF response. The sympathetic system has two main effector pathways: direct organ-targeted noradrenergic innervation and hormonal secretion from the adrenal gland. Experiments supporting the sympathetic nature of the anti-inflammatory reflex are based on observations that both β-blockers and splanchnic nerve transection increase the TNF response, yet these not only interfere with direct noradrenergic signaling but also negatively impact adrenal gland function. Meanwhile, endotoxin administration causes hyperglycemia; however, the role of the sympathetic nervous system in this process remains unclear. Additionally, most experimental approaches exploring sympathetic responses are conducted in anesthetized animals, where the sympathetic response is changed. Therefore, we examined the effect of i.v. LPS administration in stress-free intact animals. Inhibiting prostaglandin synthesis with indomethacin and blocking β-adrenergic receptors with propranolol caused increased TNF levels and prevented LPS-induced hyperglycemia, without affecting the Corticosterone response. Adrenal de-medullated animals (AdMX) receiving LPS lacked a hyperglycemic response and had higher circulating TNF levels. Intravenous adrenaline, but not noradrenaline administration in AdMX, recovered hyperglycemia and reduced TNF responses after LPS. Prostaglandin administration induced hyperglycemia in Sham but not in AdMX animals, showing that prostaglandins require the adrenal to promote acute biological effects <em>in vivo</em>. These findings demonstrate a critical role for the adrenal medulla and adrenaline in the efferent arm of the anti-inflammatory reflex, inhibiting TNF secretion and promoting hyperglycemia, thus fueling the body's defenses during an acute immune challenge.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101183"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146038515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Stress-Neuroendocrine-Myeloid Inflammation Axis Is Associated with the Progression of Ménière's Disease","authors":"Xiaofei Li ,&nbsp;Na Zhang ,&nbsp;Yongdong Song ,&nbsp;Tongtong Zhang ,&nbsp;Yafeng Lyu ,&nbsp;Huirong Jian ,&nbsp;Yawei Li ,&nbsp;Jing Wang ,&nbsp;Wenjuan Li ,&nbsp;Yinghui Hu ,&nbsp;Zhaomin Fan ,&nbsp;Na Li ,&nbsp;Daogong Zhang ,&nbsp;Haibo Wang","doi":"10.1016/j.bbih.2026.101193","DOIUrl":"10.1016/j.bbih.2026.101193","url":null,"abstract":"<div><h3>Background</h3><div>Ménière disease (MD) is a chronic inner ear disorder of unknown etiology. Although an immune-inflammatory link is suspected, the upstream triggers and cellular mechanisms connecting psychosocial stress to inner ear pathology remain poorly defined. This study aimed to investigate the role of stress-related, myeloid cell-derived inflammation in the progression of MD.</div></div><div><h3>Methods</h3><div>This multi-cohort study involved 384 MD patients (62.5% female); and 138 healthy controls (HCs) (46.4% female). Perceived stress was evaluated in 110 MD patients and 65 HCs. Transcriptional profiles were characterized using RNA sequencing on peripheral whole blood (4 MD, 6 HC) and on sorted CD11b + myeloid cells versus CD11b-non-myeloid cells (8 MD, 6 HC). In a larger cross-sectional cohort (239 MD patients, 35 HCs), the association between serum inflammatory cytokines and audio-vestibular function was examined, with a subset (n = 42) followed up. Finally, in vitro experiments explored the regulatory effects of catecholamines and glucocorticoids on myeloid cells isolated from 23 MD patients and 26 HCs.</div></div><div><h3>Results</h3><div>MD patients reported significantly higher levels of perceived stress compared to controls. RNA sequencing of peripheral blood revealed a distinct pro-inflammatory transcriptional signature in MD patients. Further analysis identified CD11b + myeloid cells as the primary source of this inflammation, showing significant upregulation of pro-inflammatory genes. Clinically, elevated serum levels of the myeloid-derived cytokine G-CSF were associated with poorer baseline audio-vestibular function, and a follow-up increase in G-CSF levels correlated with functional deterioration. Mechanistically, MD patients exhibited elevated plasma norepinephrine and increased β1-adrenergic receptor mRNA in myeloid cells. In vitro, blockade of the β-adrenergic-cAMP pathway attenuated pro-inflammatory cytokine production in these cells. Although systemic cortisol levels remained unchanged, the glucocorticoid receptor sensitivity of myeloid cells in MD patients was altered.</div></div><div><h3>Conclusion</h3><div>Our study elucidates a potential pathophysiological axis in MD, where perceived psychosocial stress is linked to sympathetic nervous system overactivity. This, in turn, primes circulating myeloid cells for a pro-inflammatory response via the β-adrenergic pathway. The resultant systemic inflammation is closely associated with the severity and progression of audio-vestibular dysfunction. These findings suggest that targeting the stress-neuroendocrine-immune interface may offer novel therapeutic strategies for MD.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"52 ","pages":"Article 101193"},"PeriodicalIF":3.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146189478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct actions of the humid heat environment on host gut microbiota, intestinal mucosal immunity, neuroendocrinology in influenza A virus-infected mouse","authors":"Sizhi Wu ,&nbsp;Yiwen Lv ,&nbsp;Peng Pang ,&nbsp;Huachong Xu ,&nbsp;Li Deng ,&nbsp;Wei Ma ,&nbsp;Xiaoyin Chen","doi":"10.1016/j.bbih.2025.101164","DOIUrl":"10.1016/j.bbih.2025.101164","url":null,"abstract":"<div><h3>Background</h3><div>Climate factors exert a profound influence on human emotional well-being and physical health. Exposure to a humid heat environment is known to precipitate anxiety-like behaviors and exacerbate the clinical manifestations of influenza; concurrently, mounting evidence has demonstrated a bidirectional regulation between the gut microbiota and human health, suggesting a potential link between environmental stress and microbial homeostasis.</div></div><div><h3>Methods</h3><div>In this study, C57BL/6J male mice were subjected to a humid heat environment for 3 weeks prior to infection with the influenza A virus. Microbiota composition, metabolites, and intestinal mucosal immunity were comprehensively measured. Furthermore, behavioral phenotypes and neurotransmitter levels were assessed to explore their potential correlations with gut dysbiosis.</div></div><div><h3>Results</h3><div>Exposure to a humid heat environment aggravated pulmonary and intestinal tissue damage while reshaping the gut microbiota composition and metabolome. This environmental stress precipitated severe pathological injury and robust inflammatory in the intestinal mucosa, characterized by a multifold upregulation of Th1/Th2-related cytokines and the suppressed expression of <em>Ocln</em>, <em>ZO-1</em>, <em>pIgR</em>, and <em>SIgA</em>. Further experiments revealed that the humid heat environment exacerbated neurological deficits in influenza A virus-infected mice, accompanied by a significant reduction in neurotransmitter levels. <strong>Conclusions</strong>: These data demonstrate that exposure to a humid heat environment exacerbates influenza infection severity through the dysregulation of the intestinal homeostasis and the neuroendocrine system, revealing the potential mechanisms underlying the digestive and nervous system symptoms observed in influenza patients.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101164"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145939223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPARγ as a predictive biomarker for antidepressant response in major depressive disorder: Insights from TNIP1 transcriptional regulation","authors":"Yu-Wei Lin ,&nbsp;Daw-Yang Hwang ,&nbsp;Yi-Yung Hung","doi":"10.1016/j.bbih.2025.101151","DOIUrl":"10.1016/j.bbih.2025.101151","url":null,"abstract":"<div><h3>Introduction</h3><div>Major depressive disorder (MDD) is a debilitating disease possibly linked to immune defense mechanisms. TNIP1, a key anti-inflammatory regulator in NF-κB and TLR pathways, is implicated in MDD, but its transcriptional regulation and role in treatment response are unclear.</div></div><div><h3>Methods</h3><div>We analyzed mRNA expression of TNIP1 and 13 transcription factors in monocytes from pre- and post-treatment (4–6 weeks) MDD patients and healthy controls. Peripheral blood mononuclear cells were isolated, tagged by CD14, and mRNA was extracted and analyzed. Participants were recruited at Kaohsiung Chang Gung Memorial Hospital (2014–2025). ANCOVA, paired t-tests, and multiple linear regression adjusted for age, gender, BMI, and smoking were used to compare groups and predict treatment outcomes.</div></div><div><h3>Results</h3><div>This study encompassed 62 MDD patients and 52 healthy controls. Pre-treatment HAMD-17 averaged 23.90 ± 4.60, and post-treatment HAMD-17 averaged 8.43 ± 4.24. MDD patients showed higher PPAR-γ (<em>p</em> &lt; 0.001), FOS (<em>p</em> = 0.023), and lower JUN (<em>p</em> = 0.029) expression than controls. Post-treatment, TNIP1 expression increased (<em>p</em> = 0.031). Lower pre-treatment PPAR-γ predicted greater symptom improvement (<em>p</em> = 0.016).</div></div><div><h3>Conclusion</h3><div>This study highlights the differential expression of PPAR-γ, FOS, and JUN in MDD patients, underscoring their potential roles in immune regulation. The association between lower pre-treatment PPAR-γ expression and improved treatment outcomes suggests its utility as a biomarker for predicting therapeutic response.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101151"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accelerated Theta Burst Stimulation Transcranial Magnetic Stimulation (iTBS-TMS) Pururauka program for severe depressive episode and suicide ideation","authors":"Hesed Virto-Farfan ,&nbsp;Carlos Virto ,&nbsp;Gustavo E. Tafet","doi":"10.1016/j.bbih.2025.101154","DOIUrl":"10.1016/j.bbih.2025.101154","url":null,"abstract":"<div><h3>Introduction</h3><div>The <em>Pururauka</em> protocol is an accelerated intermittent theta burst stimulation (iTBS) paradigm designed to rapidly reduce depressive symptoms and suicidal ideation in individuals with severe major depressive episodes. This study evaluated its clinical effects in patients presenting with insufficient response to at least two prior pharmacological treatments, current suicidal ideation, and more than two previous suicide attempts.</div></div><div><h3>Methods</h3><div>Thirty-six adults with non-psychotic major depressive disorder (ICD-11) and HAM-D-17 scores &gt;20 received a five-day accelerated iTBS intervention (180,000 pulses total) targeting the left dorsolateral prefrontal cortex. Depressive symptoms were assessed using the HAM-D and MADRS at baseline, daily during treatment, and at 1-, 3-, and 6-month follow-ups. Suicidal ideation was evaluated with HAM-D item 3 across the same time points. Satisfaction was measured with a visual analogue scale (VAS). Safety assessments included EEG screening and neuropsychiatric evaluations. Ethical approval was obtained from the Andean University of Cusco Ethics Committee (INFORME 023-2024-CIEI-UAC).</div></div><div><h3>Results</h3><div>Mean HAM-D scores decreased from 38.89 at baseline to 13.61 at day 5 and 12.36 at six months (p &lt; 0.001). Suicidal ideation resolved in most participants by day 3 and remained minimal or absent during follow-up. MADRS scores showed similar patterns, with 68 % of participants presenting no depressive symptoms immediately after treatment. No serious adverse events occurred, and satisfaction scores remained high throughout the protocol.</div></div><div><h3>Conclusion</h3><div>The <em>Pururauka</em> accelerated iTBS protocol was associated with rapid and sustained reductions in depressive symptoms and suicidal ideation in individuals with severe depressive episodes and insufficient response to previous medications. These preliminary findings warrant confirmation in future randomized controlled trials.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"51 ","pages":"Article 101154"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}