BMC Neuroscience最新文献

{"title":"High-intensity interval training modulates neural oscillations and inter-regional connectivity in college students.","authors":"Huipeng Lei, Zixuan Guo, Talifu Zikereya, Lulu Chen, Jiazheng Peng, Zhongshu Shao, Kaixuan Shi","doi":"10.1186/s12868-026-01012-7","DOIUrl":"10.1186/s12868-026-01012-7","url":null,"abstract":"<p><strong>Background: </strong>High-intensity interval training (HIIT) has been proposed as a time-efficient strategy to enhance brain health, yet its longer-term neural signatures remain unclear.</p><p><strong>Methods: </strong>In a randomized, assessor-blinded, parallel-group study, 32 healthy undergraduates (18-25 years) completed either 8 weeks of supervised HIIT (30 min/session, 3 sessions/week) or a usual-activity control. Body composition was measured before and after the intervention, and maximal oxygen uptake (VO₂max) was assessed using the 20-m shuttle run test (20 m SRT). Resting-state EEG was recorded at baseline and post-intervention. Power spectral density (PSD) and phase-based connectivity were quantified across canonical frequency bands.</p><p><strong>Results: </strong>HIIT increased VO₂max and skeletal muscle mass and reduced body fat percentage compared with baseline, while no meaningful changes were observed in controls. Resting-state EEG showed increased delta-theta-alpha power and inter-regional phase synchronization, alongside reduced beta-gamma power/connectivity.</p><p><strong>Conclusions: </strong>8 weeks of HIIT were associated with frequency-specific modulation of cortical oscillations and large-scale functional coupling at rest. These findings suggest that time-efficient exercise paradigms may promote neural network reorganization, with potential benefits for cognitive and motor function.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148027048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effects of sulfasalazine in experimental model of seizures and epilepsy.","authors":"Sree Lalitha Bojja, Gangadhar Hari, Ilora Bandyopadhyay, Kiran Kumar Kolathur, Mallikarjuna Rao Chamallamudi","doi":"10.1186/s12868-026-01007-4","DOIUrl":"10.1186/s12868-026-01007-4","url":null,"abstract":"<p><p>Overexpression of Sxc-, a cystine/glutamate antiporter is implicated in several neurological disorders including epilepsy. Physiologically, it regulates the hippocampal synaptic glutamate pool, influencing the neuronal excitability. Sulfasalazine (SAS) recently garnered interest owing to its system xc- (Sxc-) inhibitory potential. Therefore, the current study investigated the effects of SAS in two distinct models, (i) maximal electroshock (MES) induced acute seizure model and (ii) Pentylenetetrazol (PTZ) induced kindling model of chronic epilepsy and associated cognitive impairment. Initially, rats treated with different doses of SAS (25- 200 mg/kg, i.p.) for 7 days were subjected to MES and observed for seizures. SAS 50 mg/kg improved the extension-to-flexion ratio (E/F ratio) in MES induced seizures and exhibited neuroprotection, whereas the higher doses failed. In another experiment, mice were treated with PTZ (35 mg/kg) on alternate days for 24 days to induce kindling. SAS (50 or 100 mg/kg, i.p.) or vehicle was administered daily, 30 min prior to each PTZ injection. Seizures were monitored for 30 min following PTZ injection. Chronic PTZ administration led to progressively increased seizure severity, culminating in generalized tonic-clonic seizures in mice. SAS 100 mg/kg treatment reduced stage 4 and 5 seizure scores and improved spatial retention memory in mice. SAS also significantly attenuated the gene expression of inflammatory cytokines, TNF-α, IL-1β, and IL-6, and mitigated neuronal damage induced by epileptic kindling. Altogether, results suggest that SAS exhibits anti-epileptic effects, reduces neuroinflammation, and alleviates cognitive dysfunction in the PTZ kindling model of epilepsy in mice.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148026986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Awareness and self-reported synesthesia related experiences among undergraduate medical students: a cross-sectional study.","authors":"Eren Ogut, Lara Genc, Emir Mustafa Buldur, Tugba Gizem Sertduser, Dila Bade Ay, Davut Demir, Merve Akkurt, Sıla Meryem Inal, Gokhan Balci, Humeyra Elifsu Ince, Aysegul Mergen","doi":"10.1186/s12868-026-01011-8","DOIUrl":"10.1186/s12868-026-01011-8","url":null,"abstract":"<p><strong>Background: </strong>Synesthesia refers to a neurological condition in which stimuli from one sensory pathway induce perception via another sensory pathway. This study evaluated self-reported synesthesia related experiences, awareness of such experiences, and other associated demographic and clinical attributes among undergraduate medical students.</p><p><strong>Methods: </strong>This cross-sectional online survey targeted 617 medical students aged 18-25 years during the 2024-2025 academic year. Data were collected using a structured questionnaire on demographics, awareness of synesthesia-related experiences, selected medical and psychological factors, and their possible relevance to education. All analyses were performed using IBM SPSS Statistics (version 25.0).</p><p><strong>Results: </strong>Among the 617 participants, 53.5% were female, and 46.5% were male. Only 31.8% of the participants reported previous familiarity with synesthesia-like associations. Self-reported experiences compatible with synesthesia-related subtypes varied across chromesthesia-related, grapheme-color-related, lexical-gustatory-related, time-space-related, and numerical-form-related items. Differences were also established based on gender for some items. Female participants more frequently reported headaches and synesthesia-related experiences, whereas male participants more often selected responses indicating no such experiences and more frequently endorsed numerical form-related items (p < 0.001). Age did not show any significant differences. Significant correlations also existed among the synesthetic subtypes, with chromesthesia exhibiting a positive correlation with grapheme-color, lexical-gustatory, time-space, and numerical form synesthetics (p < 0.001).</p><p><strong>Conclusion: </strong>Awareness of synesthesia was low among the medical students in this study. Although some participants reported experiences compatible with synesthesia-related phenomena, these results do not confirm the prevalence of synesthesia. Instead, they described patterns of self-reported synesthesia-related experiences in an undergraduate medical student sample. Future studies using validated diagnostic and consistency-based tools are needed to determine the true frequency and educational relevance of confirmed synesthesia among medical students.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurobehavioral deficits, oxidative dysregulation, and inflammatory responses in male Swiss mice following sub-acute exposure to ethanol extract of Leiotrametes lactinea Berk.","authors":"Oyindamola O Abiodun, Tolulope B Olowoporoku, Ayomide A Ajibewa, Chinwe B Ofudi, Ifejesu V Adeniyi, Precious U Ezurike","doi":"10.1186/s12868-026-01009-2","DOIUrl":"10.1186/s12868-026-01009-2","url":null,"abstract":"<p><strong>Background: </strong>Leiotrametes lactinea (Berk.) Welti & Courtec. a mushroom reported to possess antimicrobial, antioxidant, antitumor and analgesic activities. However, there is limited information on its safety profile in the central nervous system. This study thus evaluates the neurotoxic effect of ethanol extract of Leiotrametes lactinea (EELL) in male Swiss mice following 30 days oral exposure.</p><p><strong>Method: </strong>Twenty-four (24) Swiss male mice were divided into 4 groups (n = 6) and orally administered EELL for 30 days at doses of 50, 100, and 200 mg/kg; the last group served as the healthy control. Neurobehavioral assessment started on the 21^st day, and on day 30, the animals were euthanised. Brain tissues were collected for biochemical assays (Superoxide dismutase, Catalase activity, reduced glutathione, malondialdehyde and acetylcholinesterase activity). Tumour necrosis factor-alpha and interleukin-6 levels were also measured.</p><p><strong>Results: </strong>There was a reduction in body weight gain of EELL administered groups (3.38 ± 0.68 - 4.28 ± 0.85 g) compared to the control group (7.21 ± 0.87 g), while relative organ weights were unaffected. Also, a significant reduction in locomotor activity and rearing behaviour was recorded with an increased anxiety-like behaviour in the extract treated groups. Cognitive performance evaluated with the Morris water maze demonstrated impaired retention, evidenced by reduced time spent in the target platform zone and increased proximity to the platform at higher doses. Biochemical evaluation of brain tissue showed pronounced oxidative stress, indicated by significant reductions in reduced glutathione (71.06 ± 4.74 - 124.36 ± 5.35 µg/mol vs 149.88 ± 7.07 µg/mol), catalase, and superoxide dismutase activities, alongside elevated malondialdehyde levels, especially at 100 and 200 mg/kg doses in comparison to the control. In addition, acetylcholinesterase activity was significantly increased in 100 and 200 mg/kg EELL treated groups compared to the control (0.121 ± 0.01 & 0.160 ± 0.01 µmol/min/g tissue vs. 0.049 ± 0.01 µmol/min/g tissue). Likewise, increased levels of pro-inflammatory cytokines (interleukin-6 and tumour necrosis factor-α) was recorded in the treated groups.</p><p><strong>Conclusion: </strong>These findings demonstrated that sub-acute exposure to EELL induces neurobehavioral deficits, oxidative stress, and neuroinflammatory responses, suggesting potential neurotoxic effects at higher doses.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13227754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural connectome changes as biomarkers of stroke recovery: a longitudinal 7T MRI study.","authors":"Esin Avci-Colak, Gitta Rohweder, Riccardo Iandolo, Giulia Bommarito, Ioanna Sandvig, Axel Sandvig","doi":"10.1186/s12868-026-01010-9","DOIUrl":"10.1186/s12868-026-01010-9","url":null,"abstract":"<p><strong>Background: </strong>Stroke leads to widespread brain connectivity changes, impacting areas both close and remote to the lesion. Post-stroke recovery dynamics are not fully understood. Investigating structural network reorganization over time can thus provide valuable information on adaptive and maladaptive neural plasticity changes on a subject-specific level.</p><p><strong>Methods: </strong>Four first-time ischemic stroke patients (3 M, aged 50-69 years) with upper-extremity motor impairment were examined using ultra-high field 7T MRI structural imaging protocols. For each patient, we performed longitudinal lesion quantification and white matter connectivity analysis at three critical timepoints associated with post-stroke recovery: within 1 week, at ~ 1 month, and at ~ 3 months. Using the structural MRI images, we generated patient-specific weighted structural connectivity matrices at each timepoint. We utilized the Schaefer-Yeo and Automated Anatomical Labeling atlases to derive both anatomical regions and resting-state networks based on pre-defined parcel assignments. We examined lesion evolution and white matter connectivity changes as disconnections, re-emerging connections, and existing connections with an increase in estimated connectivity strength over time. We further conducted exploratory edge-level analyses to examine the connectivity strength changes for each patient.</p><p><strong>Results: </strong>Across all patients and timepoints, an increase in estimated connectivity strength of pre-existing connections dominated structural reorganization. Temporally, the four patients revealed distinct neural reorganization patterns. Patient 1 exhibited robust structural changes in the late ~1 to ~ 3 months stage, whereas Patient 2 in the early < 1 week to ~ 1 month stage. Patient 3 had continuous network growth, while Patient 4 demonstrated stable network reorganization. In our sample, the somatomotor and attention networks underwent the most dynamic reorganization. Somatomotor and salience/ventral attention regions exhibited increased connectivity strength, and in cortical stroke cases, dorsal attention regions demonstrated decreased connectivity strength.</p><p><strong>Conclusions: </strong>In this longitudinal case series, post-stroke neural network reorganization appears to be driven by an increase in estimated connectivity strength of surviving white matter connections, suggesting compensatory neuroplasticity. Adaptive changes were most evident in the somatomotor and salience/ventral attention networks within this sample, while the dorsal attention network suggested a more limited contribution to adaptive network changes. Individual differences in the timing and pattern or reorganization highlight the potential need for further research into personalized treatment approaches to promote adaptive recovery.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13220373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147939607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ibogaine induces juvenile-like plasticity and modulates functional and structural regulators of plasticity in the adult mouse visual cortex.","authors":"Alejo Acuña, Federico Billeri, Valentino Totaro, Ignacio Carrera, Juan M Mesa, Tommaso Pizzorusso, Francesco M Rossi","doi":"10.1186/s12868-026-01005-6","DOIUrl":"10.1186/s12868-026-01005-6","url":null,"abstract":"<p><strong>Background: </strong>Psychedelics have emerged as powerful modulators of neural plasticity, yet whether the atypical psychedelic ibogaine can enhance plasticity remains poorly understood. Here, we investigated whether a single administration of ibogaine can reinstate juvenile-like experience-dependent plasticity in the adult mouse visual cortex, a canonical model for studying neuroplasticity.</p><p><strong>Results: </strong>Adult mice were treated with ibogaine (40 mg/kg, i.p.) or vehicle, and 24 h later subjected to 4 days of monocular deprivation (MD). Behavioral visual acuity was quantified using the optomotor response test, and structural plasticity was assessed through dendritic spine density analysis following Golgi staining. Ibogaine alone did not alter visual acuity or dendritic spine density in non-deprived adults. However, when coupled with MD, ibogaine restored youthful levels of plasticity: MD significantly reduced visual acuity in the deprived eye and decreased dendritic spine density in the binocular visual cortex of ibogaine-treated, but not vehicle-treated, adult mice. To examine mechanistic correlates of these findings, we quantified perineuronal nets (PNNs), parvalbumin-positive interneurons (PVs), and inhibitory synaptic puncta labeled with the vesicular GABA transporter (vGAT). We found that ibogaine reduced PNN and PV staining intensity and density, decreased the proportion of PVs enwrapped by PNNs, and lowered vGAT-positive puncta density.</p><p><strong>Conclusions: </strong>These results show that ibogaine re-establishes experience-dependent plasticity in the adult visual cortex and that this effect is accompanied by reductions in structural and inhibitory \"brakes\" on plasticity. Our findings suggest that ibogaine's long-lasting therapeutic actions can arise, at least partially, from its ability to re-open windows of heightened cortical adaptability.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147926152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural and emotional responses to mood induction and emotional design in multimedia learning.","authors":"Duygu Mutlu-Bayraktar, Ahmet Murat Uzun, Bulent Yilmaz","doi":"10.1186/s12868-026-01006-5","DOIUrl":"10.1186/s12868-026-01006-5","url":null,"abstract":"<p><p>This study investigates the effect of external mood induction and emotional design on learning and cognitive and affective outcomes in multimedia learning environments. Eye tracking and neuroimaging (EEG) methods were utilized to examine cognitive processes more thoroughly. Two different multimedia learning materials with and without emotional design were developed. Students induced with different emotional states (positive and neutral) at the beginning of the process learned the topic with the materials. The study employed a 2 × 2 factorial design between subjects with factors of emotion induction (positive induction vs. neutral) and emotional design (multimedia with emotional and multimedia with neutral design). One hundred seventeen students participated in the study. Results revealed no significant differences in learning outcomes (retention and transfer) and eye-tracking data across the groups, while a significant difference in beta waves was observed. It was found that either positive emotion induction or positive emotional design was sufficient to reduce negative emotional states. Specifically, a significant reduction in negative emotions was observed in all conditions providing at least one form of affective support, whether external (mood induction) or internal (design). Based on the results, we postulate that emotional manipulations had only a limited effect on cognitive and effective outcomes.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13255382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preventive effect of PC-SOD on oxaliplatin-induced peripheral neuropathy in rats.","authors":"Zhiwei Qiao, Yuki Uchihara, Naohiro Tsukiyama, Shota Akimoto, Noriko Kaji, Koichiro Fukuda, Tohru Mizushima","doi":"10.1186/s12868-026-01004-7","DOIUrl":"10.1186/s12868-026-01004-7","url":null,"abstract":"<p><p>BACKGROUND: Oxaliplatin is widely used as a chemotherapeutic agent for treating various cancers, including colorectal cancer. However, oxaliplatin-induced peripheral neuropathy diminishes the quality of life of patients. Thus, the development of preventive or therapeutic drugs for oxaliplatin-induced peripheral neuropathy is urgently needed. Herein, we aimed to investigate whether PC-SOD, a derivative of SOD with higher stability in plasma and higher affinity for tissues, could prevent oxaliplatin-induced peripheral neuropathy. RESULTS: PC-SOD significantly attenuated oxaliplatin-induced neurite damage and reduced oxaliplatin-induced reactive oxygen species (ROS) production in cultured PC12 cells. In a rat model, PC-SOD reduced oxaliplatin-induced mechanical allodynia, cold hyperalgesia, and morphological damage to intraepidermal nerve fibers and dorsal root ganglion. Furthermore, PC-SOD did not significantly affect the antitumor effects of oxaliplatin in cultured tumor cells or in tumor cell-implanted mice. CONCLUSION: These findings indicated that PC-SOD alleviated oxaliplatin-induced mechanical allodynia, cold hyperalgesia, and neural damage without significantly affecting the antitumor activity of oxaliplatin. Therefore, PC-SOD is a promising drug candidate for the prevention of oxaliplatin-induced peripheral neuropathy.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13235170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pretreatment with the psychedelic DOI mitigates LPS-induced hippocampal inflammation and behavioral impairments in mice.","authors":"Michael Fiorillo, Javier González-Maeso","doi":"10.1186/s12868-026-01003-8","DOIUrl":"10.1186/s12868-026-01003-8","url":null,"abstract":"<p><p>BACKGROUND: Neuroinflammation is a hallmark of numerous neuropsychiatric and neurodegenerative disorders. Psychedelics have garnered recent attention for their anti-inflammatory and neuroprotective effects. However, it remains unknown whether they can prophylactically prime immune pathways to prevent subsequent neuroinflammatory responses, and whether such effects depend on serotonin 5-HT2A receptor (5-HT2AR) signaling. METHODS: To characterize the inflammatory time-course, wild-type (WT) male mice received LPS (1 mg/kg, i.p.) and hippocampi were collected 2, 4, 6, 8, or 24 h later. In a separate WT cohort, basal cytokine effects of the psychedelic (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) were examined following administration of varying doses or vehicle, with tissue collected 24 h later. For prophylactic studies, WT and 5-HT2AR-KO mice were pretreated with DOI (0.3 or 1 mg/kg) or saline 24 h before LPS challenge. Behavioral assays included locomotor activity, the forced swim test (FST), and body weight monitoring. Hippocampal cytokines (IL-6, TNF-α, IFN-γ, IL-5, IL-4, IL-10, IL-13, IL-2) were quantified with a multiplex bead-based assay, and correlations between cytokine levels and FST immobility were assessed. RESULTS: LPS induced robust hippocampal increases in IL-6 and TNF-α and produced sickness-related behavioral deficits. DOI pretreatment (0.3 mg/kg, and to a lesser extent 1 m/kg) attenuated LPS-evoked IL-6 and TNF-α elevations, restored locomotor activity, reduced FST immobility, and accelerated recovery of body weight. These anti-inflammatory effects were partially preserved in 5-HT2AR-KO mice, indicating both receptor-dependent and receptor-independent mechanisms. Notably, 5-HT2AR-KO mice displayed exaggerated cytokine responses to LPS relative to WT animals. Correlation analyses revealed a positive association between hippocampal IL-6 levels and depressive-like behavior, whereas IL-13 and IL-2 levels were inversely correlated with immobility time in the FST. CONCLUSIONS: Prophylactic DOI administration establishes a sustained neuroimmune state that mitigates subsequent hippocampal inflammation and behavioral impairments, through mechanisms that are partially dependent on 5-HT2ARs. These findings suggest that serotonergic psychedelics can prime neural-immune interactions to confer long-lasting resilience against neuroinflammatory insults, offering a potential framework for developing next-generation psychedelic therapeutics with prophylactic anti-inflammatory and neuroprotective efficacy in neuropsychiatric and neurodegenerative disorders.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Milk-derived miR-126-3p-loaded small extracellular vesicles attenuate amyloid-β-induced cellular stress in a neuroblastoma cell model.","authors":"Sinan Gönüllü, Şeyma Aydın, Hamit Çelik, Oğuz Çelik, Sefa Küçükler, Ahmet Topal, Ramazan Akay, Mustafa Onur Yıldız, Bülent Alım, Selçuk Özdemir","doi":"10.1186/s12868-026-01002-9","DOIUrl":"10.1186/s12868-026-01002-9","url":null,"abstract":"<p><p>Alzheimer’s disease (AD) is characterized by progressive neurodegeneration driven by amyloid-β (Aβ)–associated oxidative stress, mitochondrial dysfunction, and dysregulated inflammatory signaling. Although microRNAs (miRNAs) represent promising regulators of these interconnected pathways, their therapeutic application is limited by instability and inefficient cellular delivery. In this study, the cytoprotective potential of milk-derived small extracellular vesicles (sEVs) loaded with miR-126-3p was evaluated in an Aβ-induced SH-SY5Y neuroblastoma cell model. sEVs were isolated and characterized according to MISEV guidelines, loaded with synthetic miR-126-3p, and administered to Aβ-induced cells. miR-126-3p–enriched sEVs significantly attenuated Aβ-induced oxidative stress, as evidenced by normalization of ROS, LDH, GPX1, MDA, and SOD levels, while naïve sEVs exerted only partial effects. At the transcriptional level, miR-126-3p delivery restored stress-responsive gene expression patterns by reducing ICAM1 and TNF-α expression and normalizing BDNF levels, reflecting modulation of neuron-intrinsic inflammatory signaling rather than tissue-level neuroinflammation. Markers of cytoskeletal and mitochondrial stress, including intracellular NfL, cytochrome c, 8-OHdG, TFAM, PINK1, and DNM1L, were also significantly reduced following miR-126-3p–loaded sEV treatment, indicating improved cellular homeostasis under amyloid stress. Furthermore, intracellular tau-related markers and Aβ1–40 accumulation were attenuated, consistent with suppression of Aβ-triggered pathological signaling cascades. Collectively, these findings demonstrate that sEV-mediated miR-126-3p delivery confers robust cytoprotective effects at the cellular level in a neuroblastoma model. While extrapolation to in vivo neurodegeneration requires caution, the results highlight milk-derived sEVs as a biocompatible and scalable platform for miRNA-based modulation of AD-relevant cellular stress pathways.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147466997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}