Brain Research最新文献

{"title":"Baicalin liposomes ameliorate cerebral ischemia-reperfusion-induced acute lung injury by modulating the inflammatory response","authors":"Yu Long ,&nbsp;Xiaoqiu Li ,&nbsp;Xiaofang He ,&nbsp;Zaishan Wang ,&nbsp;Yuanyuan Wu ,&nbsp;Limiao Sun ,&nbsp;Yin Ma ,&nbsp;Jie Deng ,&nbsp;Yue Hu ,&nbsp;Nan Li","doi":"10.1016/j.brainres.2025.149642","DOIUrl":"10.1016/j.brainres.2025.149642","url":null,"abstract":"<div><div>Stroke is the leading cause of death globally, with stroke-associated pneumonia being a major contributor to its high mortality. Among these complications, cerebral ischemia–reperfusion injury-induced acute lung injury (CIR-ALI) is characterized by high morbidity and mortality rate, which causes a great economic burden to the society. The course of CIR-ALI is complex, in which the inflammatory cascade response plays a central role in the pathogenesis of CIR-ALI. Baicalin (BA), a flavonoid extracted from the natural plant <em>Scutellaria baicalensis</em>, exhibits diverse pharmacological effects, including anti-inflammatory and antioxidant properties. In this study, we investigated the therapeutic effects of baicalin and its delivery system baicalin liposome (BA-LP) on CIR-ALI injury. Using in vitro models of BV2 and Raw264.7 cells, as well as an in vivo model established via the wire bolus method, we measured inflammatory factors and pathological injuries in brain and lung tissues to evaluate the intervention effects of BA and BA-LP. In addition, the preliminary analysis of network pharmacology combined with experimental validation in this study preliminarily elucidated that BA and BA-LP may attenuate CIR-ALI by modulating the PI3K/AKT/mTOR pathway.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1859 ","pages":"Article 149642"},"PeriodicalIF":2.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848703","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":"Neuroprotection in pentylenetetrazol kindling rat model: A synergistic approach with eugenol and photobiomodulation","authors":"Haitham S. Mohammed ,&nbsp;Dalia H. Ahmed ,&nbsp;Yasser A. Khadrawy ,&nbsp;Noha G. Madian","doi":"10.1016/j.brainres.2025.149645","DOIUrl":"10.1016/j.brainres.2025.149645","url":null,"abstract":"<div><div>Epilepsy is a complex neurological disorder characterized by recurrent seizures, significantly impacting patient health and quality of life. This study explores the neuroprotective effects of combining Eugenol (EUG), a natural bioactive compound administered at 100 mg/kg, with photobiomodulation (PBM), a non-invasive low-level laser therapy at 830 nm wavelength and 100 mW power, in a pentylenetetrazole (PTZ) kindling rat model of epilepsy. Fifty-nine adult male Wistar rats were assigned to five experimental groups: Control, PTZ (epilepsy model), PBM, EUG, and EUG + PBM. Seizure severity was assessed using a modified Racine scale following each PTZ injection. The study also evaluated cortical and hippocampal levels of brain-derived neurotrophic factor (BDNF), oxidative stress markers (MDA, NO, and GSH), activities of acetylcholinesterase (AChE) and Na + K + -ATPase, and monoamine neurotransmitters (DA, 5-HT, and NE). The results demonstrated that EUG and PBM, both individually and combined, significantly reduced seizure severity, mitigated oxidative stress, restored enzyme activities, and elevated BDNF levels. The combined treatment yielded superior neuroprotective effects compared to individual interventions, emphasizing its potential as a promising therapeutic strategy for epilepsy management.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149645"},"PeriodicalIF":2.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143844355","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 HIF-1α silencing in late pregnancy hypoxia-induced autism-like behavior in rat offspring","authors":"Jinghua Tang,&nbsp;Ying Yang,&nbsp;Ping Qu,&nbsp;Jie Chen,&nbsp;Tingyu Li,&nbsp;Ying Dai","doi":"10.1016/j.brainres.2025.149633","DOIUrl":"10.1016/j.brainres.2025.149633","url":null,"abstract":"<div><div>Autism spectrum disorder (ASD) is a neurodevelopmental disorder that can be caused by a variety of factors. Our previous study indicated that hypoxia-inducible factor 1 alpha (HIF-1α) plays a role in hypoxia-caused autism-like behavior. In this study, we investigated the mechanism by which HIF-1α contributes to prenatal hypoxia-induced autism-like behavior in vivo to provide an experimental basis for the treatment of ASD. We established a prenatal hypoxia model of pregnant rats by placing 17-day pregnant rats into a self-made hypoxia chamber filled with a nitrogen containing 10 %±0.5 % oxygen. Within 24 h after birth, the lateral ventricles of the prenatal hypoxia offspring rats were injected with a recombinant adeno-associated virus designed to silence HIF-1α expression. The autistic behavior of offspring rats in the HIF-1α silenced group was significantly alleviated compared with that of the prenatal hypoxia group. With the silencing of HIF-1α, the activity of phosphatase and tensin homolog (PTEN) increased and the PI3K/AKT pathway was inhibited by negative feedback. The mRNA expression level of vascular endothelial growth factor (VEGF) was decreased in the Si-HIF-1α silenced group and N-methyl D-aspartate receptor subtype 2 (NR2A) expression was downregulated. Thus, our study indicates that HIF-1α plays a role in hypoxia-induced autism-like behavior, and its regulatory effect may be achieved by inhibiting the activity of PTEN, resulting in activation of the PI3K signaling pathway. Synaptic plasticity regulation may also be involved.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149633"},"PeriodicalIF":2.7,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855347","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":"Melatonin protects mouse hippocampal neurons from neurotoxicity induced by amyloid β-peptide25–35","authors":"Karen del Carmen B. Salgado,&nbsp;Rosiene G.F. Nascimento,&nbsp;Ana Luiza S. Albuquerque,&nbsp;Laser A.M. Oliveira,&nbsp;Katiane de Oliveira Pinto Coelho Nogueira","doi":"10.1016/j.brainres.2025.149637","DOIUrl":"10.1016/j.brainres.2025.149637","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a complex neurodegenerative disorder and the leading cause of dementia in the elderly, as classified by the WHO. Its neuropathological hallmarks include the accumulation of amyloid-β (Aβ) plaques and intracellular tau tangles, which contribute to oxidative stress, mitochondrial dysfunction, lipid peroxidation, and neuronal death. Emerging evidence suggests that melatonin, a potent antioxidant produced by the pineal gland, plays a neuroprotective role in AD, yet its precise mechanisms remain underexplored. In this study, we utilized a physiologically relevant primary culture of hippocampal neurons to investigate melatonin’s protective effects against toxicity induced by Aβ25–35. Our findings demonstrate that melatonin significantly enhances cellular metabolism and viability while reducing reactive oxygen species (ROS) levels and lipid peroxidation, thereby mitigating Aβ-induced neurotoxicity. These results provide mechanistic insights into melatonin’s antioxidative and neuroprotective properties, reinforcing its potential as a therapeutic agent against oxidative stress in AD. This study underscores the promise of melatonin-based interventions in the development of novel antioxidant-targeted therapies for AD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1859 ","pages":"Article 149637"},"PeriodicalIF":2.7,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848310","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":"Corrigendum to “Sensitivity and reliability of fNIRS to detect cochlear implant-induced auditory cortical activation in prelingually deaf children with inner ear malformation or cochlear nerve deficiency” [Brain Res. 1856 (2025) 149578]","authors":"Hiroshi Yamazaki ,&nbsp;Saburo Moroto ,&nbsp;Tomoko Yamazaki ,&nbsp;Rinko Tamaya ,&nbsp;Naoko Fujii ,&nbsp;Keizo Fujiwara ,&nbsp;Yasushi Naito","doi":"10.1016/j.brainres.2025.149615","DOIUrl":"10.1016/j.brainres.2025.149615","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149615"},"PeriodicalIF":2.7,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799774","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":"USP7 promotes PINK1/Parkin-dependent mitophagy to ameliorate cerebral ischemia–reperfusion injury by deubiquitinating and stabilizing SIRT1","authors":"Dan Hou,&nbsp;Yujie Hu,&nbsp;Tian Yun,&nbsp;Dan Yu,&nbsp;Guoshuai Yang","doi":"10.1016/j.brainres.2025.149638","DOIUrl":"10.1016/j.brainres.2025.149638","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Cerebral ischemia–reperfusion (CI/R) injury, a major complication of ischemic stroke, is characterized by mitochondrial dysfunction and neuronal apoptosis, and understanding its underlying molecular mechanisms is essential for the development of effective therapeutic strategies. This study aimed to investigate the role of ubiquitin-specific protease 7 (USP7) in CI/R injury and elucidate its regulatory mechanisms.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) and an &lt;em&gt;in vitro&lt;/em&gt; neuronal model subjected to oxygen-glucose deprivation/reperfusion (OGD/R) were used to mimic CI/R injury. USP7 was overexpressed or knocked down, with or without co-treatment, using the autophagy inhibitor 3-methyladenine (3-MA). Neurological function was evaluated using standardized scoring systems, and cerebral infarct volume was quantified by TTC staining. Histopathological changes in the cortex and hippocampus were assessed using hematoxylin-eosin (HE) and Nissl staining. Neuronal viability and apoptosis were measured by CCK-8 assay, TUNEL staining, and flow cytometry. To assess cellular metabolism and oxidative stress, ATP and LDH levels, along with antioxidant markers (including SOD, GSH, and GSH-Px), were analyzed using commercial biochemical kits. Mitochondrial morphology and autophagosome formation were visualized using transmission electron microscopy. Gene and protein expression levels were quantified by qRT-PCR and Western blotting, respectively. Immunofluorescence microscopy was performed to evaluate the subcellular localization of target proteins and co-localization with mitochondrial membrane markers. Lastly, protein–protein interactions and ubiquitination modification were analyzed by co-immunoprecipitation assays.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;USP7 overexpression significantly alleviated neurological deficits, reduced infarct volume, attenuated histological damage, and decreased neuronal apoptosis in the MCAO/R model. Similarly, in the OGD/R model, USP7 overexpression markedly enhanced neuronal viability, suppressed apoptosis, restored ATP production, improved antioxidant capacity (as evidenced by increased levels of SOD, GSH, and GSH-Px), and reduced LDH release. Mechanistically, USP7 stabilized SIRT1 protein expression through deubiquitination, which in turn activated the PINK1/Parkin pathway and enhanced mitophagy. This activation was demonstrated by an increased LC3II/LC3I ratio, elevated ATG5 expression, enhanced co-localization of Tomm20 and Parkin, and increased autophagosome formation. Moreover, these protective effects were abolished when either 3-MA treatment was applied or SIRT1/PINK1 expression was knocked down.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;USP7 mitigates CI/R injury by promoting PINK1/Parkin-dependent mitophagy through SIRT1 deubiquitination and stabilization, suggesting USP7 as a potential therapeutic target for ischemic stroke.&lt;/d","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149638"},"PeriodicalIF":2.7,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143828152","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":"Hyperglycemia as driver of glioblastoma progression: Insights from Mendelian randomization and single-cell transcriptomics","authors":"Jin Li ,&nbsp;Wenjing Wu ,&nbsp;Liguo Ye ,&nbsp;Bo Zheng","doi":"10.1016/j.brainres.2025.149636","DOIUrl":"10.1016/j.brainres.2025.149636","url":null,"abstract":"<div><h3>Background</h3><div>Hyperglycemia and diabetes may influence GBM progression by altering tumor metabolism and the tumor microenvironment. However, the causal relationship between blood glucose levels and GBM remains unclear.</div></div><div><h3>Methods</h3><div>Mendelian randomization (MR) analysis was performed using GWAS data from the UK Biobank and FinnGen databases, with fasting blood glucose, plasma glucose, cerebrospinal fluid (CSF) glucose, and diabetes as exposures. Single-cell RNA sequencing of GBM mouse models on high-glucose and control diets was conducted to explore the cellular landscape of the tumor microenvironment under hyperglycemic conditions. Additionally, gene set enrichment analysis (GSEA) was performed on transcriptomic data from brain tissues of diabetic patients to assess the activity of GBM-related pathways.</div></div><div><h3>Results</h3><div>MR analysis demonstrated a significant genetic relationship between elevated fasting blood glucose and GBM risk, with an odds ratio (OR) of 40.991 (95 % CI: 2.066–813.447, p = 0.015). Type 2 diabetes (T2D) also showed a potential causal link with GBM, with the Weighted Median and Inverse Variance Weighted methods yielding ORs of 2.740 (95 % CI: 1.033–7.273, p = 0.043) and 2.100 (95 % CI: 1.029–4.287, p = 0.042), respectively. Single-cell transcriptomic analysis of GBM mouse models revealed an increased proportion of GBM tumor stem cells and pro-tumorigenic M2 macrophages in the high-glucose diet (HGD) group. GSEA of diabetic patient brain tissue revealed heightened activity of GBM-related pathways, particularly in astrocytes, endothelial cells, and neurons.</div></div><div><h3>Conclusion</h3><div>These findings suggest that hyperglycemia may actively contribute to GBM progression by promoting cellular changes within the tumor microenvironment and activating GBM-related pathways in brain tissues.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149636"},"PeriodicalIF":2.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143814683","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":"PursuitNet: A deep learning model for predicting competitive pursuit-like behavior in mice","authors":"Qiaoqian Wei ,&nbsp;Jincheng Wang ,&nbsp;Guifeng Zhai ,&nbsp;RuiQi Pang ,&nbsp;Haipeng Yu ,&nbsp;Qiyue Deng ,&nbsp;Xue Liu ,&nbsp;Yi Zhou","doi":"10.1016/j.brainres.2025.149634","DOIUrl":"10.1016/j.brainres.2025.149634","url":null,"abstract":"<div><div>Predator-prey interactions exemplify adaptive intelligence refined by evolution, yet replicating these behaviors in artificial systems remains challenging. Here, we introduce PursuitNet, a deep learning framework specifically designed to model the competitive, real-time dynamics of pursuit-escape scenarios. Our approach is anchored by the Pursuit-Escape Confrontation (PEC) dataset, which records laboratory mice chasing a magnetically controlled robotic bait programmed to evade capture. Unlike conventional trajectory datasets, PEC emphasizes abrupt speed changes, evasive maneuvers, and continuous mutual adaptation. PursuitNet integrates a lightweight architecture that explicitly models dynamic interactions and spatial relationships using Graph Convolutional Networks, and fuses velocity and acceleration data to predict change using Temporal Convolutional Networks. In empirical evaluations, it outperforms standard models such as Social GAN and TUTR, exhibiting substantially lower displacement errors on the PEC dataset. Ablation experiments confirm that integrating spatial and temporal features is crucial for predicting the erratic turns and speed modulations inherent to pursuit-escape behavior. Beyond accurate trajectory prediction, PursuitNet simulates pursuit events that closely mirror real mouse-and-bait interactions, shedding light on how innate drives, rather than external instructions, guide adaptive decision-making. Although the framework is specialized for rapidly shifting trajectories, our findings suggest that this biologically inspired perspective can deepen understanding of predator–prey dynamics and inform the design of interactive robotics and autonomous systems.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149634"},"PeriodicalIF":2.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838457","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":"GFOD1 regulates oxidative stress-induced damage in ADHD via NF-κB signaling pathway","authors":"Meng-ling Zheng ,&nbsp;Zhi-hong Yang ,&nbsp;Bin He ,&nbsp;Xin Sun ,&nbsp;Yu-ting Zhan ,&nbsp;An-qi Shao ,&nbsp;Yu-chen Hong ,&nbsp;Cai-xin Yin ,&nbsp;Ming-zheng Wang ,&nbsp;Ying-chun Ba ,&nbsp;Pin Ye","doi":"10.1016/j.brainres.2025.149605","DOIUrl":"10.1016/j.brainres.2025.149605","url":null,"abstract":"<div><div>Attention-deficit/hyperactivity disorder (ADHD) is a mental behavioral disorder that poses a serious health risk. Oxidative stress, which damages the function of neurons and astrocytes, has been discovered as a key factor contributing to ADHD pathology. A newly identified gene, Glucose-fructose oxidoreductase domain 1 (GFOD1), may be linked to the development of ADHD. It plays a role in regulating oxidative stress in ADHD; however, its exact role is unclear. This manuscript investigates the changes of GFOD1 expression and aim to correlate this with oxidative stress induced by NF-κB signaling pathway in the rat brains with ADHD and in vitro astrocytes. Our results revealed an increase in GFOD1 expression in the prefrontal cortex and cerebellar cortex of rats with ADHD, accompanied by neuronal injury and increased glial fibrillary acidic protein (GFAP) expression in astrocytes, concomitant with activation of the NF-κB p65/NOX2 signaling pathway. Along with this, GFOD1 overexpression in astrocytes resulted in an up-regulation of this signaling pathway similarly. Both ADHD rats and astrocytes in overexpressing GFOD1 showed elevated levels of reactive oxygen species (ROS) and Malondialdehyde (MDA), reduced activity of superoxide dismutase (SOD). Furthermore, treatment with the methylphenidate (MPH) did not affect GFOD1 expression. But it impacted the levels of oxidative stress mediated by the NF-κB p65/NOX2 signaling pathway. Overall, it is suggested that GFOD1 may contribute to increased levels of oxidative stress specifically in the prefrontal cortex and cerebellar cortex regions and astrocytes affected by ADHD via up-regulation of the NF-κB p65/NOX2/oxidative stress axis.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149605"},"PeriodicalIF":2.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821052","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":"Collaborative multitasking framework for enhanced hippocampus segmentation and Alzheimer’s disease classification","authors":"Lingling Fang,&nbsp;Xin Fu,&nbsp;Yongcheng Yu,&nbsp;Deshan Liu","doi":"10.1016/j.brainres.2025.149610","DOIUrl":"10.1016/j.brainres.2025.149610","url":null,"abstract":"<div><div>The early diagnosis of Alzheimer’s disease has faced significant challenges, as the initial patients have hidden symptoms that are difficult to distinguish from conventional symptoms. In view of this, this article designs a collaborative multitasking algorithm framework that implements a positive feedback loop between classification tasks, significantly improving processing accuracy. Specifically, the algorithm consists of three sub networks: the initial segmentation sub network accurately identifies the hippocampus boundary and generates the initial segmentation mask; The classification subnetwork relies on initial segmentation information to effectively distinguish different stages of Alzheimer’s disease; Finally, the fine segmentation sub network finely adjusts the contour of the hippocampus based on the classification results. To verify the superiority of this method, this study used 269 MRI sample of Alzheimer’s disease patients, including clinical and public datasets. The experimental results demonstrate that the proposed method exhibits superior performance in both hippocampal classification and segmentation tasks. Specifically, in terms of segmentation, the method achieved an average Dice Similarity Coefficient (DSC) of 94.0% and a Jaccard Index (JA) of 80.6%. For classification tasks, the method demonstrated an accuracy (AC) of 98.8%, sensitivity (SEN) of 98.8%, specificity (SP) of 98.6%, and F1 score (F1) of 97.8%, collectively indicating excellent clinical performance.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149610"},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143808503","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}