IBRO Neuroscience Reports最新文献

{"title":"Research trends and hot spots in obesity-induced pain: A bibliometric analysis of the last 20 years","authors":"Lei Gao ,&nbsp;Yazhou Wen ,&nbsp;Kunlin Guo,&nbsp;Renqi Li,&nbsp;Mao Mao,&nbsp;Shanwu Feng,&nbsp;Xian Wang","doi":"10.1016/j.ibneur.2025.02.001","DOIUrl":"10.1016/j.ibneur.2025.02.001","url":null,"abstract":"<div><h3>Background</h3><div>Obesity can directly lead to allodynia, increase the incidence of chronic pain, and aggravate existing pain. However, the mechanisms underlying obesity-related or obesity-induced pain are still not understood. Herein, we performed a comprehensive bibliometric analysis of obesity-related or obesity-induced pain, aiming to analyze the current trends and hot spots as well as explore the underlying mechanisms.</div></div><div><h3>Methods</h3><div>We searched reviews and articles on obesity-related or obesity-induced pain from 2005 to 2024 via the Web of Science Core Collection (WoSCC) database. We subsequently conducted bibliometric analysis employing WPS Office, a web-based bibliometric analysis platform (<span><span>https://bibliometric.com</span><svg><path></path></svg></span>), VOSviewer, Pajek, and CiteSpace.</div></div><div><h3>Results</h3><div>In total, 347 papers were identified for bibliometric analysis. The country, institution, and journal with the greatest influence were the USA, Albert Einstein College of Medicine, and Headache, respectively. Dr. Lipton RB and Dr. Karppinen J were the top 2 influential authors on the basis of their significant number of publications and citations. The keywords for the latest burst were \"inflammation,\" \"risk,\" \"neuropathic pain,\" \"gene-related peptide,\" \"knee osteoarthritis,\" and \"validation.\" Notably, the article titled \"The association between chronic obesity and pain\" by Okifuji A received the highest number of citations as well as the strongest citation burst. He and colleagues noted a significant correlation between obesity and pain in terms of clinical manifestations, but this connection is indirect and is modulated by certain biomechanical and structural alterations linked to obesity, inflammatory agents, mood disorders, sleep disturbances, and lifestyles.</div></div><div><h3>Conclusion</h3><div>There has been a notable surge in the number of articles published in the last two decades. The investigation into neuroendocrine and neuroimmune mechanisms underlying obesity-related or obesity-induced pain is expected to be a hot spot in the coming years. A potential strategy for treating chronic obesity and pain should pay attention to particular endocrine regulators, inflammatory cytokines, or immune cells that serve as central elements or crucial signaling pathways within this regulatory system.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 311-322"},"PeriodicalIF":2.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143395145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association between NLGN4 gene variants and the incidence of autism spectrum disorders in Guilan, Iran","authors":"Sepideh Atefrad ,&nbsp;Aidi Yousefnejad ,&nbsp;Niloofar Faraji ,&nbsp;Parvaneh Keshavarz","doi":"10.1016/j.ibneur.2025.01.018","DOIUrl":"10.1016/j.ibneur.2025.01.018","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) is a developmental disorder characterized by impaired social interaction, communication skills, and repetitive behaviours. This study aimed to investigate the association between variants of the Neuroligin-4 (NLGN4) gene (rs1882260 and rs3810688) and the incidence of ASD in North of Iran in the ASD group (n = 60) and control group (n = 60). DNA was isolated from whole blood, saliva, or hair samples. The targeted variants were genotyped using the Amplification Refractory Mutation System-Polymerase Chain Reaction (ARMS-PCR) technique. Genetic analyses were conducted using SNPAlyze ver. 8.1. Results revealed a significant difference of rs3810688 polymorphism in the NLGN4 gene in both genotypic and allelic frequency distributions between the ASD and control groups (P &lt; 0.05). The GG genotype of rs3810688 polymorphism exhibited a significant association with an elevated risk of ASD in contrast to the CC genotype, as revealed under the co-dominant model (OR=4.2; 95 %CI, 1.25–14.05; P = 0.019). The study illustrated the possible role of rs3810688 polymorphism of NLGN4 in increasing the incidence of ASD among newborns in Guilan province. Also, the G-C haplotype was found to be a protective variant against ASD.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 306-310"},"PeriodicalIF":2.0,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143395146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adherent junctions: Physiology, role in hydrocephalus and potential therapeutic targets","authors":"Zhiye Chen ,&nbsp;Jian He ,&nbsp;Yating Guo ,&nbsp;Yue Hao ,&nbsp;Wentao Lv ,&nbsp;Zexin Chen ,&nbsp;Junqiang Wang ,&nbsp;Yijian Yang ,&nbsp;Kaiyue Wang ,&nbsp;Zhikun Liu ,&nbsp;Qian Ouyang ,&nbsp;Zhangjie Su ,&nbsp;Pingsheng Hu ,&nbsp;Gelei Xiao","doi":"10.1016/j.ibneur.2025.02.003","DOIUrl":"10.1016/j.ibneur.2025.02.003","url":null,"abstract":"<div><div>In all epithelial cells, the adherent junctions (AJs) with cadherin as the core play an important role in the maintenance of the connection and the formation of apical-basal polarity. The ependymal cells close to the ventricular system rely on AJs with N-cadherin at the core to maintain their normal morphology and function. Therefore, it has an important impact on the function and disease of the central nervous system. Hydrocephalus is a pathological phenomenon of excessive cerebrospinal fluid accumulating in the ventricular system accompanied by continuous ventricular dilatation, which can be divided into obstructive hydrocephalus and communicating hydrocephalus according to the pathogenesis. Obstructive hydrocephalus is often associated with excessive ependymal cells produced by differentiation of radial glial cells. The etiology of communicating hydrocephalus is mainly related to the dyskinesia of cerebrospinal fluid. In addition, the damage of the brain barrier can lead to brain edema and aggravate the symptoms. At present, the researches on the pathogenesis of hydrocephalus are mainly focused on the development of ependymal cells and cilia, while less attention has been paid to molecules such as AJs, which play an important role in maintaining the polarity of ependymal cells. This paper discusses the formation and function of AJs and their role in preventing hydrocephalus by preserving the polarity of ependymal cilia, regulating the number of ependymal cells, and upholding the brain barrier integrity to impede hydrocephalus exacerbation, which provides a new direction for the study of hydrocephalus.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 283-292"},"PeriodicalIF":2.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143349536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conditioned medium derived from mesenchymal stem cells and spinal cord injury: A review of the current therapeutic capacities","authors":"Gholam Reza Kaka ,&nbsp;Farrokh Modarresi","doi":"10.1016/j.ibneur.2025.02.004","DOIUrl":"10.1016/j.ibneur.2025.02.004","url":null,"abstract":"<div><div>Spinal cord injury (SCI) is a debilitating condition of the nervous system that imposes considerable challenges for subjects, such as bladder and bowel incontinence and infections. The standard therapeutic strategy is methylprednisolone utilization accompanied by surgical decompression. However, achieving an effective therapy with the minimum side effects for SCI is still a puzzle. Nowadays, mesenchymal stem cell (MSC) therapy has received much consideration in scientific communities in light of its pharmacological and therapeutic properties, for instance, anti-inflammatory, regenerative, analgesic, and immunomodulatory influences. Despite the mentioned advantages for MSCs, their tumorigenic potential is a limiting agent for its wide therapeutic application. Recent documents show that the use of conditioned medium (CM) derived from MSCs can largely solve these problems. CM encompasses neuroprotective growth factors and cytokines, such as stem cell factor (SCF), vascular endothelial growth factor (VEGF), and glial cell line-derived neurotrophic factor (GDNF). The persuasive evidence from experimental studies revealed that CM originating from MSCs can have a considerable role in the amelioration of SCI. Hence, in the current papers, we will review and summarize evidence indicating the anti-SCI mechanisms of MSC-derived CM by relying the current experimental data.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 293-299"},"PeriodicalIF":2.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143378164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the roles and clinical potential of exosome-derived non-coding RNAs in glioma","authors":"Peng Jin ,&nbsp;Xue Bai","doi":"10.1016/j.ibneur.2025.01.015","DOIUrl":"10.1016/j.ibneur.2025.01.015","url":null,"abstract":"<div><div>Non-coding accounts for 98 %-99 % of the human genome and performs many essential regulatory functions in eukaryotes, involved in cancer development and development. Non-coding RNAs are abundantly enriched in exosomes, which play a biological role as vectors. Some biofunctional non-coding RNAs are specifically designed as exosomes for the treatment of cancers such as glioma. Glioma is one of the most common primary tumors within the skull and has varying degrees of malignancy and histologic subtypes of grades I-IV. Gliomas are characterized by high malignancy and an abundant blood supply due to rapid cell proliferation and vascularization, often with a poor prognosis. Exosomal non-coding RNAs can be involved in the tumorigenesis process of glioma from multiple directions, such as angiogenesis, tumor proliferation, metastatic invasion, immune evasion, apoptosis, and autophagy. Therefore, non-coding RNAs in exosomes are suitable as markers or therapeutic targets for early diagnosis of diseases and for predicting the prognosis of a variety of diseases. Regulating exosome production and the level of exosomal non-coding RNA expression may be a new approach to prevent or eliminate glioma. In this review, we review the origin and characteristics of exosomal non-coding RNAs, and introduce the functional studies of exosomal non-coding RNAs in glioma and their potential clinical applications, in order to broaden new ideas for the treatment of glioma.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 323-337"},"PeriodicalIF":2.0,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143420583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing Alzheimer's Therapy: Computational strategies and treatment innovations","authors":"Jibon Kumar Paul ,&nbsp;Abbeha Malik ,&nbsp;Mahir Azmal ,&nbsp;Tooba Gulzar ,&nbsp;Muhammad Talal Rahim Afghan ,&nbsp;Omar Faruk Talukder ,&nbsp;Samar Shahzadi ,&nbsp;Ajit Ghosh","doi":"10.1016/j.ibneur.2025.02.002","DOIUrl":"10.1016/j.ibneur.2025.02.002","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a multifaceted neurodegenerative condition distinguished by the occurrence of memory impairment, cognitive deterioration, and neuronal impairment. Despite extensive research efforts, conventional treatment strategies primarily focus on symptom management, highlighting the need for innovative therapeutic approaches. This review explores the challenges of AD treatment and the integration of computational methodologies to advance therapeutic interventions. A comprehensive analysis of recent literature was conducted to elucidate the broad scope of Alzheimer's etiology and the limitations of conventional drug discovery approaches. Our findings underscore the critical role of computational models in elucidating disease mechanisms, identifying therapeutic targets, and expediting drug discovery. Through computational simulations, researchers can predict drug efficacy, optimize lead compounds, and facilitate personalized medicine approaches. Moreover, machine learning algorithms enhance early diagnosis and enable precision medicine strategies by analyzing multi-modal datasets. Case studies highlight the application of computational techniques in AD therapeutics, including the suppression of crucial proteins implicated in disease progression and the repurposing of existing drugs for AD management. Computational models elucidate the interplay between oxidative stress and neurodegeneration, offering insights into potential therapeutic interventions. Collaborative efforts between computational biologists, pharmacologists, and clinicians are essential to translate computational insights into clinically actionable interventions, ultimately improving patient outcomes and addressing the unmet medical needs of individuals affected by AD. Overall, integrating computational methodologies represents a promising paradigm shift in AD therapeutics, offering innovative solutions to overcome existing challenges and transform the landscape of AD treatment.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 270-282"},"PeriodicalIF":2.0,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143349535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive analysis of MAPT-related genetic risk in Alzheimer’s disease","authors":"Shitao Wang ,&nbsp;Guoshuai Luo ,&nbsp;Xiangqian Ding ,&nbsp;Guangxin Sun ,&nbsp;Mengen Zhang ,&nbsp;Jingjing Dong ,&nbsp;Hui Xu ,&nbsp;Jinghong Lu ,&nbsp;Zongyou Li ,&nbsp;Bin Ning ,&nbsp;Hongbo Liu","doi":"10.1016/j.ibneur.2025.01.017","DOIUrl":"10.1016/j.ibneur.2025.01.017","url":null,"abstract":"<div><div>Despite some research into the correlation between microtubule associated protein tau (<em>MAPT</em>) rs2471738 and the risk of AD, the findings remain inconclusive. The aim of this study was to explore the association between <em>MAPT</em> rs2471738 and the susceptibility to AD, as well as potential molecular mechanisms involved. We conducted a comprehensive literature search on Embase, Medline, and Web of Science to investigate the relationship between <em>MAPT</em> rs2471738 and the risk of AD. We employed meta-analysis and Expression Quantitative Trait Loci analysis to elucidate the association between <em>MAPT</em> rs2471738 and AD risk, as well as to uncover potential molecular mechanisms. Aggregated results suggest that the rs2471738T allele increases the risk of developing AD under the allelic model (odds ratio [OR] = 1.15, 95 % confidence interval [CI] = 1.04–1.26, I² = 64.9 %). Additionally, our findings indicate that the rs2471738CT+TT genotype escalates the risk of AD under the dominant model (OR = 1.23, 95 % CI = 1.07–1.41, I² = 79.2 %). Moreover, rs2471738 regulates the expression of <em>MAPT</em> in the human hippocampus (<em>P</em> = 0.04). Our result suggested that rs2471738 may potentially increase the risk of AD by modulating the expression of <em>MAPT</em> in human brain tissue.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 300-305"},"PeriodicalIF":2.0,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143386926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N-acetyl cysteine through modulation of HDAC2 and GCN5 in the hippocampus mitigates behavioral disorders in the first and second generations of socially isolated mice","authors":"Najmeh Asgharzadeh ,&nbsp;Ali Noori Diziche ,&nbsp;Hossein Amini-Khoei ,&nbsp;Nasrin Yazdanpanahi ,&nbsp;Mehrdad Shahrani Korrani","doi":"10.1016/j.ibneur.2025.01.014","DOIUrl":"10.1016/j.ibneur.2025.01.014","url":null,"abstract":"<div><h3>Objective(s)</h3><div>Social isolation stress (SIS) in early life can lead to behavioral disorders. N-acetylcysteine (NAC), an antioxidant, may aid treatment. This study explored NAC's impact on behavior in first and second-generation mice after SIS, focusing on HDAC2 and GCN5 expression in the hippocampus.</div></div><div><h3>Materials and methods</h3><div>In this study, 24 male and 24 female mice were bred for one generation. The pups were divided into six (3male, 3female) groups (n = 20): 1- Control receiving normal saline, 2- SIS with normal saline, 3- SIS with NAC (150 mg/kg) IP for four weeks. Eight mice from each group underwent behavioral, histopathological, and molecular tests, while others were mated (4 males + 4 females) to produce second generations. These pups were divided into 9 groups (n = 8) for behavioral tests, including elevated plus maze, open field, forced swimming, and histopathological and molecular assessments (HDAC2 and GCN5 expression) in the hippocampus.</div></div><div><h3>Results</h3><div>The SIS group showed increased HDAC2 and GCN5 expression. Following SIS, there was a decrease in open arm entries and passes in the open field test, alongside increased immobility in the forced swimming test and reduced CA1 and CA3 hippocampal diameters. NAC mitigated the adverse molecular, behavioral, and histopathological impacts of SIS across both generations.</div></div><div><h3>Conclusion</h3><div>NAC reduces behavioral disorders after SIS (first and second generation) by reducing the expression of GCN5 and HDAC2 and increasing neuronal diameter in the hippocampus. Future research should investigate the long-term therapeutic effects of NAC for behavioral disorders after SIS.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 350-359"},"PeriodicalIF":2.0,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the effect and mechanism of Shaoyao Gancao Decoction in the treatment of pain in Parkinson's disease using network pharmacology and molecular docking","authors":"Zhaohui Xu ,&nbsp;Qing Zhao","doi":"10.1016/j.ibneur.2025.01.013","DOIUrl":"10.1016/j.ibneur.2025.01.013","url":null,"abstract":"<div><div>This study explores the potential effects and mechanisms of SGD in treating pain in PD based on network pharmacology and molecular docking technology.The chemical components in the aqueous extract from SGD were identified using GC-MS analysis. A prediction network describing the relationship between SGD and pain in PD was established based on information collected from multiple databases. Using Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Geomes (KEGG) pathway enrichment of key target genes in the DAVID6.8 database to obtain treatment target genes. To further investigate the molecular interactions, AutoDock Vina were employed to perform molecular docking and visualize the resulting outcomes. There were 206 targets obtained from the 105 active ingredients in Paeoniae Radix Alba and Radix Rhizoma Glycyrrhizae, and 5110 disease targets related to pain in PD were identified. GO enrichment analysis indicates that its Biologica Process (BP) involve response to lipopolysaccharide, response to metal ion. Cellular Component (CC) analysis suggests its primary impact on various membrane structural components. Molecular Function (MF) enrichment results primarily include ubiquitin-like protein ligase binding. KEGG pathway enrichment mainly encompasses MAPK, AGE-RAGE, IL-17, TNF, and Toll-like receptor signaling pathways. According to the results of molecular docking, the binding activity between core components and targets was marvelous (affinity &lt; −5.0 kcal/mol). SGD has more advantages in the regulation of various types of pain in PD through multiple targets, which is worthy of further study.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 200-210"},"PeriodicalIF":2.0,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143093396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Postnatal expression of Cat-315-positive perineuronal nets in the SAMP10 mouse primary somatosensory cortex","authors":"Hiroshi Ueno ,&nbsp;Yu Takahashi ,&nbsp;Sachiko Mori ,&nbsp;Eriko Kitano ,&nbsp;Shinji Murakami ,&nbsp;Kenta Wani ,&nbsp;Yosuke Matsumoto ,&nbsp;Motoi Okamoto ,&nbsp;Takeshi Ishihara","doi":"10.1016/j.ibneur.2025.01.012","DOIUrl":"10.1016/j.ibneur.2025.01.012","url":null,"abstract":"<div><div>Perineuronal nets (PNNs) form at the end of the critical period of plasticity in the mouse primary somatosensory cortex. PNNs are said to have functions that control neuroplasticity and provide neuroprotection. However, it is not clear which molecules in PNNs have these functions. We have previously reported that Cat-315-positive molecules were not expressed in the PNNs of the senescence-accelerated model (SAM)P10 strain model mice at 12 months of age. To confirm whether the loss of Cat-315-positive molecules occurred early in life in SAMP10 mice, we examined Cat-315-positive PNNs in the primary somatosensory cortex during postnatal development. This research helps to elucidate the function of PNNs and the mechanism of cognitive decline associated with ageing. To confirm whether Cat-315-positive PNNs changed in an age-dependent manner in SAMP10 mice, we examined the primary somatosensory cortex at 21, 28, and 56 days after birth. We compared these results with those of senescence-accelerated mouse-resistant (SAMR) mice. In SAMP10 mice, Cat-315-positive PNNs were expressed in the primary somatosensory cortex early after birth, but their expression was significantly lower than that in SAMR1 mice. Many other molecules that calibrated the PNN were unchanged between SAMP10 and SAMR1 mice. This study revealed that the expression of the Cat-315 epitope was decreased in the primary somatosensory cortex of SAMP10 mice during postnatal development. SAMP10 mice have had histological abnormalities in their brains since early life. Furthermore, using SAMP10 will be useful in elucidating the mechanism of age-related abnormalities in brain function as well as in elucidating the function and structure of PNNs.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 244-256"},"PeriodicalIF":2.0,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143093497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}