Journal of Neuroscience Research最新文献

{"title":"Protective Effect of Resveratrol Against Intracranial Aneurysm Rupture in Mice","authors":"Dung Ngoc Phuong Dang,&nbsp;Yoshinobu Kamio,&nbsp;Toru Kawakatsu,&nbsp;Hiroshi Makino,&nbsp;Kazuya Hokamura,&nbsp;Ryo Imai,&nbsp;Yasuhito Suzuki,&nbsp;Hisaya Hiramatsu,&nbsp;Liu Zhitong,&nbsp;Kazuo Umemura,&nbsp;Kazuhiko Kurozumi","doi":"10.1002/jnr.70059","DOIUrl":"https://doi.org/10.1002/jnr.70059","url":null,"abstract":"<div>\u0000 \u0000 <p>Resveratrol is a polyphenol and potent antioxidant that has anti-inflammatory effects in conditions such as atherosclerosis, aortic aneurysm, and inflammatory bowel disease. In this study, we investigated whether resveratrol exerts anti-inflammatory effects and protects against intracranial aneurysm formation and rupture in male mice. Intracranial aneurysms were induced in mice using a combination of elastase injection into the cerebrospinal fluid and deoxycorticosterone acetate-salt (DOCA-salt)-induced hypertension. Male mice were divided into two groups: a resveratrol diet group and a normal diet group. The dietary intervention lasted for 6 weeks, starting 3 weeks prior to elastase injection. The overall incidence of aneurysms did not differ significantly between the normal diet and resveratrol diet groups (71% vs. 59%, <i>p</i> = 0.497). However, resveratrol significantly reduced the rate of aneurysmal rupture compared with that in the normal diet group (88% vs. 40%, <i>p</i> = 0.026). Furthermore, resveratrol supplementation increased the mRNA levels of Sirtuin 1 (<i>Sirt1</i>) and decreased the mRNA levels of nuclear factor kappa B subunit 1 (<i>Nfkb1</i>) and Tumor necrosis factor (<i>Tnf</i>). Our findings demonstrate that resveratrol reduces intracranial aneurysm rupture in a mouse model, indicating its therapeutic potential in this condition.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abnormal Static and Dynamic Functional Connectivity in Tension-Type Headache: A Support Vector Machine Analysis","authors":"Mengting Li,&nbsp;Shuxian Zhang,&nbsp;Fan Chu,&nbsp;Yan Zhan,&nbsp;Mengqi Zhao,&nbsp;Zeqi Hao,&nbsp;Linlin Zhan,&nbsp;Jun Ren,&nbsp;Xize Jia","doi":"10.1002/jnr.70057","DOIUrl":"https://doi.org/10.1002/jnr.70057","url":null,"abstract":"<div>\u0000 \u0000 <p>Tension-type headache (TTH) is a primary headache with the highest prevalence. Previous studies have revealed the local brain abnormalities of TTH patients. However, little is known about its brain connectivity disruption. Based on rs-fMRI data from 33 TTH patients and 30 healthy controls (HCs), static functional connectivity (FC) and dynamic FC were calculated between the default mode network (DMN) and the whole brain. Regions of interest (ROIs)-wise FC was performed to explore the connectivity pattern of the circuit established by the static and dynamic FC methods. The support vector machine (SVM) model was applied to distinguish the TTH patients from HCs. Compared with the HCs, TTH patients showed increased FC between the left posterior cingulate cortex (PCC) and the left parahippocampal and left middle frontal gyrus (MFG). Decreased dynamic FC was observed between the left PCC and right middle occipital gyrus (MOG), left precuneus, left inferior parietal gyrus (IPG), right median cingulate and paracingulate gyri (DCG) and right supplementary motor area (SMA) in TTH patients. The ROI-wise FC results showed that left precuneus-left IPG, left precuneus-right DCG, and left IPG-right SMA generated higher FC in TTH patients. SVM obtained a total accuracy of 70.476%, and the area under the curve (AUC) value was 0.658. TTH patients showed abnormal static and dynamic connectivity in multiple brain regions, and abnormal brain activity was also identified within these brain regions. This novel classification model using the brain connectivity could be useful in detecting neuro-markers for clinical applications in TTH patients.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abscisic Acid Enhances Motor and Cognitive Function in the 3-Acetylpyridine Mouse Model of Cerebellar Ataxia","authors":"Monavareh Soti,&nbsp;Mehran Ilaghi,&nbsp;Hoda Ranjbar,&nbsp;Kristi A. Kohlmeier,&nbsp;Mansoureh Sabzalizadeh,&nbsp;Mohammad Shabani","doi":"10.1002/jnr.70055","DOIUrl":"https://doi.org/10.1002/jnr.70055","url":null,"abstract":"<div>\u0000 \u0000 <p>Cerebellar ataxia is a debilitating neurodegenerative disorder characterized by impaired motor coordination and balance with limited treatment options. Abscisic acid (ABA), a phytohormone detected in mammalian brains, has shown neuroprotective properties. This study investigated the effects of ABA on motor, cognitive, and affective deficits in a mouse model of cerebellar ataxia in which male Swiss mice received a single intraperitoneal injection of 3-acetylpyridine (3-AP; 60 mg/kg), which leads to the loss of climbing fiber input to Purkinje neurons leading to cerebellar degeneration. In ABA-treated groups, ABA (10 or 15 μg/mouse) was intracerebroventricularly applied for four consecutive days. Behavioral testing consisted of open field, footprint analysis, wire grip, rotarod, tail suspension, elevated plus maze, Morris water maze, and the passive avoidance assay. Cerebellar brain-derived neurotrophic factor (BDNF) levels were measured using ELISA. As expected, 3-AP-treated mice exhibited significant motor impairments, increased anxiety-like and depressive-like behaviors, and cognitive deficits. ABA treatment, particularly at the 15 μg/mouse dose, significantly improved motor coordination, locomotor activity, memory, and spatial and passive avoidance learning as well as reduced anxiety-like and depressive-like behaviors. Behavioral changes were associated with normalization of the 3-AP-induced increases in cerebellar BDNF levels. This study demonstrates that ABA can ameliorate motor, cognitive, and affective deficits in a mouse model of cerebellar ataxia, which could involve BDNF and be due to neuroprotective effects in the cerebellum. By extension, our data suggest that ABA may have therapeutic potential in the management of cerebellar ataxia and other cerebellar disorders.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144292849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Attention Regulation Among Sleep-Deprived Air-Force Pilots","authors":"Talya Dolev,&nbsp;Inon Maoz,&nbsp;Salman Zubedat,&nbsp;Shlomit Aga-Mizrachi,&nbsp;Anna Levkovsky,&nbsp;Idan Nakdimon,&nbsp;Oded Ben-Ari,&nbsp;Dan Grinstein,&nbsp;Barak Gordon,&nbsp;Avi Avital","doi":"10.1002/jnr.70052","DOIUrl":"https://doi.org/10.1002/jnr.70052","url":null,"abstract":"<p>Short sleep duration is associated with adverse physical and mental events. However, it is quite challenging to objectively quantify its impact on human cognitive performance. Thus, we aim to examine the effects of sleep deprivation on physiological measures of emotional and attention regulation, in terms of recovery dynamics among sleep-deprived air force pilots. Ninety-one pilots participated in a sleep deprivation workshop held by an aeromedical center. The Auditory Sustained Attention Test (ASAT) and the Psychomotor Vigilance Test were applied to evaluate emotional and attention performance at baseline, post 24-h of sleep deprivation, following recovery of 3- and 8-h of sleep. Machine learning was used to predict the aerial professions based on the physiological measures. The results indicate that 24 h of sleep deprivation induced impairments in both attention and emotional regulation; however, while 3 h of sleep recovery have ameliorated emotional regulation and latency to response inhibition, attention performance required 8 h of sleep to ameliorate the observed 70% impairment. The physiologically measured adverse effects induced by sleep deprivation were distinctive among aerial professions, thus allowing machine learning prediction with high accuracy, sensitivity, and specificity. The effects of sleep-deprivation-induced fatigue were detected by the ASAT measures, which may be utilized as an objective, non-invasive physiological measure to quantify emotional and attention regulation. The ability to monitor sleep effects in a fast and accurate manner may be beneficial for the competence assessment of pilots and promote safety, and the differentiation across the aerial professions may potentially improve individual suitability assessment, together with the consequences of sleep deprivation.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Executive Function Decline and Its Association With TNF-α in the Later Stages of Post-Acute Sequelae of COVID","authors":"Aditi Varenya,&nbsp;K. Vijayalakshmi,&nbsp;Mythri Rajeswara Babu","doi":"10.1002/jnr.70051","DOIUrl":"https://doi.org/10.1002/jnr.70051","url":null,"abstract":"<div>\u0000 \u0000 <p>Beyond the immediate impact of the COVID-19 pandemic, survivors often grapple with incapacitating post-infection symptoms, referred to as Post-Acute Sequelae of COVID (PASC) when persistent beyond 90 days. Cognitive manifestations, encompassing attention, memory, and executive functions (EF), collectively termed brain fog, contribute to functional challenges in PASC. This infection also elicits a long-lasting pro-inflammatory response that persists even after viral clearance, potentially correlated with brain fog. However, it is unclear whether pro-inflammatory responses and cognitive sequelae persist beyond 1 year after the onset of infection. Thus, this study sought to investigate the long-term consequences of PASC on EFs as well as a potential association with markers of inflammation. Forty individuals with PASC who passed performance validity testing (PVT) and 40 matched healthy controls (HC) underwent neuropsychological assessments, including the Montreal Cognitive Assessment to assess global cognition, Victoria Stroop Test to assess inhibitory control, Wisconsin Card Sorting Test to assess cognitive flexibility, Digit Span Task to assess working memory, and Mackworth Clock Test to assess sustained attention on the Psychology Experiment Building Language (PEBL) toolkit. Serum was assayed for tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10). Results indicate significant EF decline in PASC, inversely correlated with serum TNF-α concentrations, approximately 562 ± 225 days after the onset of infection. Thus, there exists protracted EF decline in PASC, persistent even beyond 1 year after the onset of infection. Increased levels of TNF-α are observed to be associated with poorer executive functioning in PASC.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenylyl Cyclase Activator: Forskolin Mediates CREB ser133 Phosphorylation in the Hippocampus, Alleviates Autism-Like Deficits in a Valproic Acid Model of Wistar Rats","authors":"Ashish Jain,&nbsp;Neha Dhir,&nbsp;Praisy K Prabha,&nbsp;Anupam Raja,&nbsp;Amit Raj Sharma,&nbsp;Tamanna Kaundal,&nbsp;Shiv Charan,&nbsp;Alka Bhatia,&nbsp;Dibyajyoti Banerjee,&nbsp;Biman Saikia,&nbsp;Deepy Zohmangaihi,&nbsp;Manoj K. Goyal,&nbsp;Bikash Medhi,&nbsp;Ajay Prakash","doi":"10.1002/jnr.70049","DOIUrl":"https://doi.org/10.1002/jnr.70049","url":null,"abstract":"<div>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by social deficits, restricted interest, and repetitive behaviors. The prevalence is higher in males (4:1). FDA-approved drugs, Aripiprazole, and risperidone, only target comorbid conditions and have significant side effects. Dysregulation in cAMP-responsive element-binding protein (CREB) signaling is reported in autistic individuals. Forskolin is traditionally used in Ayurvedic medicine with lesser side effects. It is a potent adenylyl cyclase (AC) activator, increases intracellular cyclic adenosine monophosphate (cAMP) levels, thereby activating the protein kinase A (PKA)/CREB pathway with clinically proven benefits as an anticancer, anti-asthmatic, and in metabolic disorder, and crosses the blood–brain-barrier (BBB) junction. The present study aimed to investigate the impact of Forskolin and sought to explore the role of estrogen beta (ERβ/ESR2) receptors in a valproic acid (VPA) model of ASD. Pregnant Wistar rats received VPA or an equal volume of saline on gestational day (GD) 12.5. From postnatal day (PND) 23, male and female rats were divided separately into control, VPA, risperidone, and Forskolin (10–30 mg/kg) groups. Systemic administration of Forskolin ameliorated anxiety, social deficit, repetitive behavior, spatial recognition memory, motor coordination, gastrointestinal (GIT) motility, brain edema, and BBB permeability in a dose-dependent manner. Moreover, chronic Forskolin treatment significantly alleviated VPA-induced neuronal damage in the prefrontal cortex (PFC), hippocampus (HC), and cerebellum, and increased the intracellular CREB ser133 protein phosphorylation. Forskolin upregulated the mRNA expression of CREB signaling, which was altered by prenatal VPA administration. Our findings indicate that Forskolin provides neuroprotection through CREB signaling, suggesting its therapeutic potential for ASD.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144197321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcription Factors and Coregulators in Schwann Cell Differentiation, Myelination, and Remyelination: Implications for Peripheral Neuropathy","authors":"Sang-Heum Han,&nbsp;Jun-Gi Cho,&nbsp;Su-Jeong Park,&nbsp;Yoon Kyung Shin,&nbsp;Young Bin Hong,&nbsp;Jin-Yeong Han,&nbsp;Hwan Tae Park,&nbsp;Joo-In Park","doi":"10.1002/jnr.70053","DOIUrl":"https://doi.org/10.1002/jnr.70053","url":null,"abstract":"<div>\u0000 \u0000 <p>Schwann cells (SCs) are required for supporting axons, forming myelin, and facilitating repair through remyelination after injury in the peripheral nervous system (PNS). Processes of differentiation, myelination, and remyelination of SCs are tightly modulated by a complex network of transcription factors and coregulators, including Sox10, Oct6/Pou3f1, Krox20/Egr2, Nab1/2, YY1, COUP-TFII/NR2F2, YAP/TAZ-TEAD1, c-Jun, Sox2, Zeb2, and Etv1/Er81. These factors can regulate the expression of essential target genes such as <i>Mpz</i> and <i>Mbp</i> in SC myelination and repair. Genetic mutations or dysregulation within this network can lead to peripheral neuropathies such as Charcot–Marie–Tooth disease. However, the transcriptional regulatory network of differentiation, myelination, and remyelination of SCs has not been fully understood yet. Thus, this review briefly introduces processes of differentiation, myelination, and remyelination of SCs and explores the role and molecular mechanisms of each transcription factor and coregulator in differentiation and myelination of SCs and their remyelination following nerve injury. Clinical implications for peripheral neuropathies associated with specific gene mutations and variations of transcription factors and coregulators affecting SC biology are also discussed.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144190673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intermittent Hypoxia Damages Tyrosine Hydroxylase-Containing Neurons in the Substantia Nigra and Locus Coeruleus but Not Hippocampal Neurons in Male Mouse Models of Early-Stage Sleep Apnea","authors":"Chia-Hui Chu,&nbsp;Yueh-Ching Chang,&nbsp;Kuang-Ting Liu,&nbsp;Yen-Chin Liu,&nbsp;Mei-Chuan Chou,&nbsp;Ching-Kuan Liu,&nbsp;Chu-Huang Chen,&nbsp;Junn-Liang Chang,&nbsp;Shiou-Lan Chen","doi":"10.1002/jnr.70050","DOIUrl":"https://doi.org/10.1002/jnr.70050","url":null,"abstract":"<div>\u0000 \u0000 <p>In sleep apnea, repeated hypovolemic ventilation or apnea in sleep leads to intermittent hypoxia (IH) of the brain. Thus, the impacts of sleep apnea on the brain need to be investigated. In this study, a mouse model with sleep-associated chronic IH and behavior tests was used to evaluate how IH impacts brain function and the expression of tyrosine hydroxylase (TH)-containing neurons in the substantia nigra, ventral tegmental area (VTA), and locus coeruleus. In an open-field test, mice subjected to chronic IH (5%–21% oxygen) for 10 and 20 days exhibited a significant decrease in spontaneous locomotor activity compared to the room air (RA, 21% oxygen) control mice. In the Y-maze test, the ability to recognize novel and familiar arms was similar between groups. In immunostaining of the brains of IH mice, TH-positive neurons in the substantia nigra, VTA, and locus coeruleus were significantly reduced compared to RA mice. Furthermore, in the brains of mice with decreased TH-positive neurons induced by IH, the expression of hippocampal neurons has not been affected. In the analysis of glial cells, in IH group mice, a significant increase of microglia was found in the substantia nigra, VTA, locus coeruleus, and hippocampus compared to the RA mice. These findings suggest that there is a loss of TH-containing neurons and neuronal inflammation in the substantia nigra, VTA, and locus coeruleus under chronic IH. Our findings provide precise evidence for the loss of TH-containing neurons in the setting of chronic IH mouse models, which can provide relevant empirical observations for clinicians.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytic HSP60 Deletion Induced Astrocyte Senescence and Inhibited Neuroregeneration via Modulating the S1P/Truncated-BDNF Pathway","authors":"Wenhui Zhu,&nbsp;Yanfang Cheng,&nbsp;Ziping Lang,&nbsp;Weifen Li,&nbsp;Xiangzan Wei","doi":"10.1002/jnr.70054","DOIUrl":"https://doi.org/10.1002/jnr.70054","url":null,"abstract":"<div>\u0000 \u0000 <p>Heat Shock Protein 60 (HSP60) plays a critical role in maintaining mitochondrial function in astrocytes and has a significant impact on central nervous system (CNS) health. However, how HSP60 regulates the mitochondrial function of astrocytes to inhibit neuroregeneration remains unknown. In this study, we generated astrocyte-specific HSP60 knockout male mice to investigate the consequences of HSP60 deficiency. Firstly, our results confirmed that HSP60 deficiency caused abnormal expression of mitochondrial function-related genes, causing significant mitochondrial dysfunction, which triggered cellular senescence in astrocytes. Moreover, the alterations of 5-hydroxytryptamine 2A receptor (5-HT2AR), glucocorticoid receptor (GR), dopamine D2 receptor (D2R), and N-methyl-D-aspartate receptor subunit 2A (NR2A) expression suggested a disruption in neurotransmission and synaptic plasticity. Additionally, the increased levels of site-1 protease (S1P), truncated brain-derived neurotrophic factor (truncated-BDNF), and synaptophysin indicate synaptic structural and functional impairments. Expectedly, our findings demonstrated mitochondrial dysfunction and cellular senescence in astrocytes, leading to altered expression of neurotransmitter receptors in the cortex, as well as reduced neuronal numbers and neurotransmitter levels in the hippocampus after the deletion of HSP60 in astrocytes of the male mice. Notably, Urolithin A (UA) and the S1P inhibitor, PF429242, were found to alleviate astrocyte senescence and promote neuronal regeneration by inhibiting truncated BDNF expression. In conclusion, our study revealed that HSP60 deficiency in astrocytes induces mitochondrial dysfunction and cellular senescence via the S1P/truncated-BDNF pathway, resulting in disrupted neurotransmitter receptor expression, synaptic protein alterations, and impaired neuroregeneration. These insights underscored the importance of HSP60 in CNS health and provided promising avenues for developing treatments for neurodegenerative disorders.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144179361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling Stress-Related Disorders in Zebrafish Using Prolonged Predator Exposure and Prolonged Unpredictable Stress","authors":"Aleksander V. Zhdanov,&nbsp;Sergey L. Khatsko,&nbsp;Konstantin N. Zabegalov,&nbsp;Maksim V. Bytov,&nbsp;Konstantin A. Demin,&nbsp;David S. Galstyan,&nbsp;Murilo S. de Abreu,&nbsp;Tamara G. Amstislavskaya,&nbsp;Allan V. Kalueff","doi":"10.1002/jnr.70048","DOIUrl":"https://doi.org/10.1002/jnr.70048","url":null,"abstract":"<div>\u0000 \u0000 <p>The neurobiology of human stress-related disorders remains poorly understood, necessitating novel models and new model organisms to advance translational research in this field. Complementing rodent studies, the zebrafish (<i>Danio rerio</i>) is a useful model species for stress-related disorders. Here, we develop two novel experimental models of stress-related brain disorders, based on repeated prolonged exposure to predators or on chronic unpredictable stress in adult zebrafish. The ability of both models to recapitulate human stress in these fish was assessed behaviorally, in the novel tank and the plus maze (anxiety, locomotor, and cognitive tests), as well as by analyzing the baseline levels of cortisol, a common neuroendocrine biomarker of stress. Overall, anxiety-like behavior in the novel tank test was seen in both stressed groups, whereas poor learning and higher anxiety were observed in the plus maze test in predator-exposed fish, paralleling clinical cognitive and affective symptoms. Elevated cortisol in both stressed zebrafish further resembled neuroendocrine deficits seen in stress-related disorders clinically. Finally, the evoked behavioral and endocrine stress symptoms were rescued by treatment with two popular, clinically active antidepressant drugs, fluoxetine and paroxetine. Collectively, these models successfully recapitulated in zebrafish several key aspects of clinical stress-related disorders, further supporting the utility of these fish for translational stress research and anti-stress drug development.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 6","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}