Brain Research最新文献

{"title":"Anxiolytic-like, anorexic, adipsogenic and anti-alcohol intake effects of acute taurine administration into dorsal periaqueductal gray of female and male adult Wistar rats","authors":"Priscila Vázquez-León ,&nbsp;Abraham Miranda-Páez","doi":"10.1016/j.brainres.2025.149720","DOIUrl":"10.1016/j.brainres.2025.149720","url":null,"abstract":"<div><div>Taurine (TAU, 2-aminoethane sulphonic acid) is a semi-essential β sulfonated amino acid, one of the most abundant free amino acids in the body and the mammalian brain. Most studies on taurine have demonstrated its beneficial role at acute doses, administered either systemically or i.c.v., on numerous disease models and an inhibition of alcohol intake. The periaqueductal gray (PAG) is a key vertebrate midbrain structure for integrated defensive responses, including those representing stress and anxiety-like behavior. A strong relationship between anxiety and alcohol intake, besides the critical role of dorsal periaqueductal gray (D-PAG) in behavioral defensive and consummatory responses, has been shown. This study aimed to assess the pharmacological effects of taurine administration into D-PAG on anxiety-like behavior through the elevated plus maze test, as well as consummatory behavior through food, water, and alcohol intake and preference. Both female and male rats, either alcohol naïve or forced ethanol intake (since juvenile age with a chronic intermittent access model), were implanted with cannulae on the right side of D-PAG. We found that administering taurine into D-PAG elicits an anxiolytic-like effect and reduces food and water intake in all groups. Furthermore, taurine inhibits alcohol consumption by adult Wistar rats previously exposed to alcohol.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1862 ","pages":"Article 149720"},"PeriodicalIF":2.7,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144116968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of pulse shape and current direction of TMS on test–retest reliability, and variability of measurement outcomes","authors":"Desmond Agboada ,&nbsp;Roman Rethwilm ,&nbsp;Wolfgang Seiberl ,&nbsp;Wolfgang Mack","doi":"10.1016/j.brainres.2025.149715","DOIUrl":"10.1016/j.brainres.2025.149715","url":null,"abstract":"<div><h3>Background</h3><div>Pulse parameters of transcranial magnetic stimulation (TMS) critically affect the stimulation outcomes. There is, however, a lack of understanding on how these parameters influence test–retest reliability and variability of single-pulse TMS protocols.</div></div><div><h3>Objectives</h3><div>This study aims to investigate the effects of four combinations of pulse shapes and current directions (TMS-waveform conditions) on outcome measurements, test–retest reliability, and variability.</div></div><div><h3>Methods</h3><div>Using robot-assisted neuronavigation, nineteen participants were stimulated with four TMS-waveform conditions in three repeated sessions within the same day. Sessions 1 and 2, and Sessions 1 and 3 were separated by 30 min, and approximately 7 h, respectively. The four TMS-waveform conditions were: biphasic and monophasic pulses delivered in either posterior-anterior (PA) or anterior-posterior (AP) current directions. TMS protocols investigated were resting/active motor thresholds, stimulus intensity for inducing 1 mV peak-to-peak motor-evoked potential (MEP) amplitude, corticospinal excitability measurements (MEP amplitudes and latencies) with three inter-stimulus intervals (ISIs) of 5, 10, and 15 s; input–output (I/O) curve, and cortical silent period.</div></div><div><h3>Results</h3><div>TMS-waveform influenced all spTMS protocol outcome measures except for the I/O. TMS pulses in the PA current direction generally induced less variable MEP amplitudes and latencies. Moderate to excellent test–retest reliability was also found for all protocols except the I/O, however TMS-waveform only influenced the reliability of the AMT and MEP latency protocols. Monophasic pulses in the PA direction were more reliable compared to pulses in AP for MEP latency, while biphasic pulses in the AP direction showed significantly lower reliability compared to other TMS-waveform conditions for the AMT.</div></div><div><h3>Conclusion</h3><div>This systematic evaluation does shed more light on protocols and TMS pulse parameters that induce reliable and less variable measurements.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1862 ","pages":"Article 149715"},"PeriodicalIF":2.7,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Texture features of T2w magnetic resonance imaging mirror tissue changes in Parkinson’s disease models","authors":"Chirine Katrib ,&nbsp;Camille Naidji ,&nbsp;David Devos ,&nbsp;Kelly Timmerman ,&nbsp;Nicolas Durieux ,&nbsp;Nathalie Dutheil ,&nbsp;Erwan Bezard ,&nbsp;Charlotte Laloux ,&nbsp;Nacim Betrouni","doi":"10.1016/j.brainres.2025.149717","DOIUrl":"10.1016/j.brainres.2025.149717","url":null,"abstract":"<div><div>After successful applications in the oncology field to provide new <em>in vivo</em> diagnosis and prognosis imaging features, texture analysis and more generally radiomics were also reported as having the potential to provide markers of different neurodegenerative processes. Indeed, in neurodegenerative diseases such as Parkinson’s disease (PD), there is a need for neuroprotective therapies, the development of which will be fundamentally aided by imaging biomarkers capable of inferring tissue changes such as loss of neurons in the nigro-striatal pathway or alpha synuclein aggregates that characterize PD. In this study, we therefore sought to decipher the relationship between signal changes measured using brain MRI texture features and histological changes in preclinical models of this disease.</div><div>Three rodent models were used: two toxin-based models, one involving 6-hydroxydopamine injection and the other using methyl-phenyl-tetrahydropyridine, and a third model based on alpha-synuclein overexpression. Animals had MR imaging with a <em>T2w</em> sequence evaluation and were sacrificed for histological analyses of the brains. Texture features were measured in different brain structures. The association analyses revealed significant correlations between the imaging features measured in the substantia nigra and the striatum with dopaminergic degeneration, as well as significant correlations between texture features in key structures (substantia nigra, striatum, thalamus, hippocampus and associative and cingulate cortices), and alpha-synuclein quantified in these regions.</div><div>These preliminary results suggest that MR signal changes captured using texture features reflect the underlying tissue changes occurring in the brain such as neuronal death and proteins accumulation.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1862 ","pages":"Article 149717"},"PeriodicalIF":2.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144107921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COMM domain containing 4 inhibits hephaestin and ferroportin to enhance neuronal ferroptosis by disturbing the Cu-Fe balance in amyotrophic lateral sclerosis","authors":"Xingli Tan ,&nbsp;Xiaoli Su ,&nbsp;Ying Wang ,&nbsp;Weiwei Liang ,&nbsp;Di Wang ,&nbsp;Di Huo ,&nbsp;Hongyong Wang ,&nbsp;Yan Qi ,&nbsp;Wenmo Zhang ,&nbsp;Ling Han ,&nbsp;Dongmei Zhang ,&nbsp;Ming Wang ,&nbsp;Jing Xu ,&nbsp;Shuyu Wang ,&nbsp;Jing Wang ,&nbsp;Honglin Feng","doi":"10.1016/j.brainres.2025.149707","DOIUrl":"10.1016/j.brainres.2025.149707","url":null,"abstract":"<div><div>Dysregulation of copper and iron homeostasis contributes to the progression of amyotrophic lateral sclerosis (ALS), but the role and mechanism of COMM domain containing 4 (COMMD4) in ALS remains unclear. In this research, we showed that the expression of COMMD4 was upregulated in ALS cells and animal models. The increased COMMD4 induced neuronal ferroptosis by disrupting the Cu-Fe balance. Mechanistic studies indicated that COMMD4 inhibited ferroportin (FPN)-mediated neuronal iron efflux by inhibiting intracellular copper and hephaestin (HEPH). Our findings demonstrated that COMMD4 depletion exerts neuroprotective effects on ALS by increasing intracellular copper and activating HEPH/FPN pathway, rather than affecting the interaction between HEPH and FPN. Targeting COMMD4 and its downstream signaling pathways may offer potential therapeutic avenues for ALS.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1861 ","pages":"Article 149707"},"PeriodicalIF":2.7,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Restoring neuronal excitability and spatial memory through inhibiting amyloid-β-induced hyperactive NF-κB in a rat model of Alzheimer’s disease","authors":"Zahra Soleimani ,&nbsp;Shima Davoudi ,&nbsp;Fatemeh Saffarzadeh ,&nbsp;Gila Behzadi ,&nbsp;Mehdi Mehdizadeh ,&nbsp;Mona Rahdar ,&nbsp;Narges Hosseinmardi ,&nbsp;Mahyar Janahmadi ,&nbsp;Mohammad J. Eslamizade","doi":"10.1016/j.brainres.2025.149703","DOIUrl":"10.1016/j.brainres.2025.149703","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder associated with aberrant neuronal activity. In AD, NF-κB, a key transcription factor and inflammatory mediator, becomes hyperactive, influencing gene expression, and likely neuronal excitability. This study investigates whether inhibiting intracortical injection of amyloid-β peptides (Aβ)-induced hyperactive NF-κB can restore spatial memory impairment and abnormal neuronal activity in rats. We observed that intracortical injection of Aβ increases immunoreactivity of phosphorylated-p65 in CA1 pyramidal neurons. We demonstrated that <em>in vivo</em> treatment of rats with JSH-23 restores anxiety-like behaviors as well as spatial learning and memory, as assessed by elevated plus maze and Morris water maze, respectively. In addition, using patch-clamp recording we showed that the intrinsic excitability of CA1 pyramidal neurons, particularly in terms of the evoked spikes, is reduced in Aβ-injected rats along with altered resting membrane properties. Incubating acute brain slices from control rats in aCSF containing JSH-23 did not influence the neuronal activity. In contrast, this incubation restored almost all of the passive- and activity-dependent properties of CA1 pyramidal neurons in brain slices from Aβ-injected rats. Furthermore, we found that Aβ-induced enhancement of Ih currents and after-hyperpolarization amplitude (AHP) are reduced by JSH-23 incubation, possibly underlying rescuing effects of NF-κB inhibition at behavioral and cognitive level. Collectively, our results suggest that hyperactive NF-κB signaling in AD is associated with abnormal neuronal activity and deficits in cognitive functions. Moreover, pharmacologic inhibition of this signaling molecule restores neuronal excitability, as well as rescues spatial memory, likely through influencing Ih currents and AHP.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1861 ","pages":"Article 149703"},"PeriodicalIF":2.7,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging the gap between structural and metabolic neuroimaging via MRI-to-PET synthesis: A tri-attention enhanced GAN approach","authors":"Jinhua Sheng ,&nbsp;Haodi Zhu ,&nbsp;Rougang Zhou ,&nbsp;Qiao Zhang ,&nbsp;Jialei Wang ,&nbsp;Ziyi Ying","doi":"10.1016/j.brainres.2025.149691","DOIUrl":"10.1016/j.brainres.2025.149691","url":null,"abstract":"<div><div>Magnetic resonance imaging (MRI) and positron emission tomography (PET) are two essential neuroimaging modalities that provide complementary structural and metabolic information about the brain, thereby enhancing diagnostic precision for brain disorders such as Alzheimer’s disease (AD). To address the limitations of missing modality data, we propose a novel 3D GAN-based framework for MRI-to-PET neuroimage synthesis, incorporating a Tri-Attention module to integrate spatial, channel, and frequency attention across multiple scales. The proposed method enables the generation of complementary metabolism information by synthesizing PET scans, effectively bridging the modality gap. The effectiveness of the proposed method is evaluated on a subset of the Alzheimer’s Disease Neuroimaging Initiative (ADNI) dataset. Experimental results demonstrate the superiority of our approach, achieving significant improvements in image quality metrics (SSIM: 0.882, PSNR: 26.508) and clinical metrics (SUVR), outperforming state-of-the-art methods. These findings underscore the potential of our framework to bridge the gap between structural and metabolic information, offering a promising tool for cross-modality neuroimage synthesis and clinical applications.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1862 ","pages":"Article 149691"},"PeriodicalIF":2.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal high-fat diet exposure impairs LKB1-TGFβ1 inflammatory pathway and increases hypothalamic 5HT receptors gene expression and somatic growth in young rats","authors":"Wenicios Ferreira Chaves ,&nbsp;Suleyma de Oliveira Costa ,&nbsp;Nilton J. Santos ,&nbsp;Melissa Santos de Aguiar ,&nbsp;Carol Fuzeti Elias ,&nbsp;Marcio Alberto Torsoni ,&nbsp;Isabeli Lins Pinheiro ,&nbsp;Raquel da Silva Aragão","doi":"10.1016/j.brainres.2025.149706","DOIUrl":"10.1016/j.brainres.2025.149706","url":null,"abstract":"<div><div>The serotonergic system regulates various psychobiological processes, including neurodevelopment, mood, and feeding behavior. Maternal exposure to a high-fat diet (HFD) increases circulating proinflammatory cytokines, impairing the development of the serotonergic system in the offspring’s brain. The effects of maternal exposure to HFD on the offspring’s feeding behavior, somatic growth, and hypothalamic serotonergic system were investigated. Wistar rat offspring from HFD-fed dams displayed increased body weight, fat mass, and somatic growth but no changes in food intake or feeding behavior. They also showed elevated total cholesterol and reduced serum creatinine. At the molecular level, increased hypothalamic gene expression of <em>Htr1a</em>, <em>Htr2a</em>, and <em>Tgfb1,</em> along with a reduction in the phosphorylation of FoxO1^Thr24, cAMP response element-binding protein (CREB^Ser133), and liver kinase B1 (LKB1^Ser428) were observed. No differences in leptin or insulin signaling were found. These results suggest an initial disruption in energy homeostasis mediated by the serotonergic system.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1862 ","pages":"Article 149706"},"PeriodicalIF":2.7,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Call category classification of the isolation-induced ultrasonic vocalizations emitted by BTBR T+Itpr3tf/J mouse pups exposed to different perinatal diets","authors":"Yan Mei Nie ,&nbsp;Aishwarya Udayan ,&nbsp;Elizabeth DiLiberto ,&nbsp;Robert Feingold ,&nbsp;Kathryn K. Chadman","doi":"10.1016/j.brainres.2025.149690","DOIUrl":"10.1016/j.brainres.2025.149690","url":null,"abstract":"<div><div>Autism spectrum disorder (ASD) is characterized by deficits in social communication and repetitive behaviors/restricted interests that may be diagnosed as early as 2 years of age. This suggests that the pathology underlying the disorder is present during early development, including gestation. This early developmental period is affected by maternal nutrition. The effects of a perinatal high fat diet on neonatal ultrasonic vocalizations (USVs) were examined in the BTBR mouse model of ASD, and C57BL/6J mice. Three diets with varied levels of fats and carbohydrates were given to dams beginning 2 weeks prior to mating through weaning. Isolation-induced USVs were recorded from the offspring at P4, P6, and P8. The spectrograms were sorted into call categories using neural networks trained with DeepSqueak. The number, duration, frequency, and power for each call category were evaluated for effects of maternal diet, age, and strain. The BTBR pups made significantly more calls than the B6 pups, regardless of diet, age, sex, or call type. The high fat diet (HFD) affected the BTBR mice more than the B6 mice, significantly increasing both the weight of the pups and the overall number of calls. Maternal diet had only small effects on the call category usage. This analysis provides information about the duration, principle frequency, and power of the different call categories employed by the BTBR and B6 pups.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1862 ","pages":"Article 149690"},"PeriodicalIF":2.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of myeloperoxidase in the pathogenesis of stroke","authors":"Wei Liu ,&nbsp;Yi-Ran Wang ,&nbsp;Hongyun Wu ,&nbsp;Wenqiang Cui ,&nbsp;Xiangqing Xu","doi":"10.1016/j.brainres.2025.149705","DOIUrl":"10.1016/j.brainres.2025.149705","url":null,"abstract":"<div><div>Stroke is the leading cause of mortality and morbidity worldwide, significantly impacting human welfare and overall health. Myeloperoxidase (MPO), a heme peroxidase secreted by neutrophils, plays a crucial role in the body’s defense mechanisms, exhibiting pro-inflammatory and pro-oxidative properties. Additionally, MPO compromises the structural integrity and functional capacity of blood vessels, potentially leading to the formation and dislodgement of atherosclerotic plaques, vascular stenosis, thrombosis, and ultimately contributing to stroke occurrence. Following a stroke, a significant influx of neutrophils infiltrates the cerebral tissue, leading to an excessive release of MPO-derived oxidants and the subsequent promotion of various inflammatory mediators, thereby exacerbating cerebral tissue damage. Numerous studies have consistently demonstrated the pivotal role of MPO in the pathogenesis and progression of stroke, establishing it as a reliable prognostic indicator. Exploring the association between MPO and stroke enhances our understanding of the pathological mechanisms underlying stroke and aids in the development of therapeutic interventions. This review provides a comprehensive analysis of the molecular structure and cellular localization of MPO, elucidating its critical role in mediating vascular injury, the formation of Neutrophil Extracellular Traps (NETs), oxidative stress, neuroinflammation, disruption of the blood–brain barrier (BBB), and neuronal apoptosis during stroke pathogenesis. Additionally, we discuss recent advancements in MPO-targeted drugs and Traditional Chinese Medicine compounds as potential therapeutic strategies for stroke treatment.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1861 ","pages":"Article 149705"},"PeriodicalIF":2.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144070834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PINK1 activation by MTK458 ameliorates neurological impairments and pyroptosis after intracerebral hemorrhage in mice","authors":"Jianliang Li ,&nbsp;Yincheng Li ,&nbsp;Zhe Chen ,&nbsp;Liang Yang ,&nbsp;Lin Zhao ,&nbsp;Jingchen Li","doi":"10.1016/j.brainres.2025.149700","DOIUrl":"10.1016/j.brainres.2025.149700","url":null,"abstract":"<div><div>Intracerebral hemorrhage (ICH) is often linked to severe neurological impairments, including cognitive deficits and anxiety-like behaviors. This study aimed to evaluate the therapeutic potential of PTEN-induced kinase 1 (PINK1), which is activated during ICH, as a target for mitigating these effects. C57/BL6 wild-type mice underwent ICH induction through an intrastriatal injection of autologous blood. The PINK1 activator, MTK458, was administered daily doses of 10–50 mg/kg starting one week before ICH induction and continuing for three days post-surgery. The modified neurological severity score (mNSS) was used to assess neurological deficits, while brain edema was measured through brain water content. The open field test and Y-maze test were used to evaluate anxiety-like behavior, and cognitive function respectively. The effects of ICH on cortical cell pyroptosis, Parkin/PINK1-mediated mitophagy, and the activation of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome were analyzed via Western blotting, ELISA, and qRT-PCR. MTK458 effectively reduced brain water content in the basal ganglia, ipsilateral cortex, and cerebellum, with improvements in mNSS extending to 14 days post-injury. Additionally, MTK458 alleviated both neurological deficits and anxiety-like behavior in ICH mouse models. It also reversed ICH-induced cortical cell pyroptosis by promoting Parkin/PINK1-mediated mitophagy and inhibiting NLRP3 inflammasome activation, as well as the expression of IL-1β and IL-18. These results suggest that MTK458 effectively reduces neurological impairments, brain edema, and anxiety-related behaviors in mice following ICH, highlighting PINK1 activation as a promising therapeutic strategy for ICH-induced neurological deficits.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1861 ","pages":"Article 149700"},"PeriodicalIF":2.7,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}