Neurobiology of Disease最新文献

{"title":"The interaction of UBR4, LRP1, and OPHN1 in refractory epilepsy: Drosophila model to investigate the oligogenic effect on epilepsy","authors":"Rui-Na Huang ,&nbsp;Si-Yuan Luo ,&nbsp;Tao Huang ,&nbsp;Xiong-Sheng Li ,&nbsp;Fan-Chao Zhou ,&nbsp;Wei-Hao Yin ,&nbsp;Ze-Ru Chen ,&nbsp;Shi-Zhan Yuan ,&nbsp;Ling-Ying Li ,&nbsp;Bin Tang ,&nbsp;Jing-Da Qiao","doi":"10.1016/j.nbd.2025.106955","DOIUrl":"10.1016/j.nbd.2025.106955","url":null,"abstract":"<div><div>Refractory epilepsy is an intractable neurological disorder that can be associated with oligogenic/polygenic etiologies. Through trio-based whole-exome sequencing analysis, we identified a clinical case of refractory epilepsy with three candidate gene variants: <em>UBR4</em>, <em>LRP1</em>, and <em>OPHN1</em>. Utilizing the Gal4-UAS system and double-balancer tool, we generated single, double, and triple knockdown <em>Drosophila</em> models to investigate the interactions of the three candidate genes. Seizure behavioral experiments combined with logistic regression analysis revealed the individual epileptogenicity and significant synergistic epileptogenic effects of the three mutations. By constructing a SHAP-XGBoost machine learning model integrating seizure behavior data with knockdown efficiency metrics, we discovered that <em>LRP1</em> mutation served as the primary effector in the oligogenic system. Based on transcriptome analysis, main related processes of oxidative stress and metabolic imbalance together with expressional dysregulation separately of 48, 52, and 43 epilepsy-associated genes were discovered to confirm the epileptogenicity of <em>OPHN1</em> knockdown, <em>UBR4-LRP1</em> knockdown, and <em>UBR4-LRP1-OPHN1</em> knockdown. Up-regulation of COX7AL and ND-B8 enriched in metabolic pathways and down-regulation of Diedel enriched in extracellular space component were indicated to be responsible for the significant epileptogenicity of the oligogenic knockdown. For this clinical instance, epileptic pharmacoresistance was considered to be triggered by a combination of KIF gene family, SLC gene family, and ASIC gene family. This study established a novel framework to clarify the multiple genetic structure of epileptogenicity in refractory epilepsy with oligogenic background, which could be critical to translational medicine and precision therapy development.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"212 ","pages":"Article 106955"},"PeriodicalIF":5.1,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty acid binding proteins and their involvement in anxiety and mood disorders","authors":"Matthew J. Jones ,&nbsp;Taygun C. Uzuneser ,&nbsp;Steven R. Laviolette","doi":"10.1016/j.nbd.2025.106952","DOIUrl":"10.1016/j.nbd.2025.106952","url":null,"abstract":"<div><div>Anxiety and mood disorders represent the most prevalent neuropsychiatric conditions. Nevertheless, current pharmacotherapies often have a host of adverse side effects. Emerging evidence suggests modulation of lipid signaling pathways – particularly those involved in the endocannabinoid (eCB) system, may offer promising new targets for the treatment of anxiety and depression. Polyunsaturated fatty acids (PUFA) and their metabolic derivatives, including the eCB ligands, have garnered significant attention for their roles in neuropsychiatric disease mechanisms. Intracellular transportation of these lipids is facilitated by fatty acid binding proteins (FABP), which are increasingly recognized as key regulators of lipid signaling. Accumulating evidence indicates that FABPs may impact the development of neuropsychiatric disorders by mediating the signaling pathways of PUFAs and eCB ligands. In this review, we investigate the role of FABPs in two major categories of neuropsychiatric conditions – anxiety disorders and clinical depression. We begin by examining several neuropathophysiological mechanisms through which FABPs can impact these conditions, focusing on their role as lipid chaperones. These mechanisms include the trafficking of eCB ligands, as well as oleoylethanolamide and palmitoylethanolamide; modulation of inflammatory responses through PUFA transport and PPAR activation; regulation of PUFA availability to support neurogenesis; influence on stress-related pathways, including NMDA receptor activation and the hypothalamic-pituitary-adrenal axis; and the facilitation of dopamine receptor trafficking and localization. Next, we discuss preclinical evidence linking FABP function to anxiety- and depression-related behaviours. Finally, we propose that pharmacologically targeting FABP-mediated pathways holds considerable potential as a novel therapeutic strategy for addressing the symptoms associated with mood and anxiety disorders.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"212 ","pages":"Article 106952"},"PeriodicalIF":5.1,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143943197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vascular depression: A comprehensive exploration of the definition, mechanisms, and clinical challenges","authors":"Siyuan Wu ,&nbsp;Yi Zhang ,&nbsp;Yingqiong Lu ,&nbsp;Yuqi Yin ,&nbsp;Chen Yang ,&nbsp;Wenjing Tang ,&nbsp;Tao Song ,&nbsp;Xi Tao ,&nbsp;Qing Wang","doi":"10.1016/j.nbd.2025.106946","DOIUrl":"10.1016/j.nbd.2025.106946","url":null,"abstract":"<div><div>Vascular depression (VaDep), which was proposed over two decades ago, is a distinct subtype of depression primarily observed in patients with stroke and cerebral small-vessel disease and is characterized by white matter hyperintensities; however, the lack of standardized diagnostic criteria and consensus limits its clinical application. This review explores the pathological conditions and vascular risk factors that may precipitate VaDep, particularly in relation to stroke and cerebral small-vessel disease. VaDep is distinguished by unique pathophysiological mechanisms and treatment responses. We categorize these mechanisms into three groups: 1) macroscopic mechanisms, including vascular aging, cerebral hypoperfusion, blood–brain barrier disruption, and neural circuit dysfunction; 2) microscopic mechanisms, involving the inflammatory response, hypothalamic–pituitary–adrenal axis dysregulation, impaired monoamine synthesis, and mitochondrial dysfunction; and 3) undetermined mechanisms, such as microbiota–gut–brain axis dysbiosis. These insights support VaDep as a distinct depression subtype, differentiating it from late-life depression and major depressive disorder. Treatment is challenging, as patients with VaDep often exhibit resistance to conventional antidepressants. Addressing vascular risk factors and protecting vascular integrity are essential for effective management. Future research should validate these mechanisms and develop novel diagnostic and therapeutic approaches to improve VaDep outcomes.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"211 ","pages":"Article 106946"},"PeriodicalIF":5.1,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WDR62 controls cortical radial migration and callosal projection of neurons in the developing cerebral cortex","authors":"Yiqiang Zhi ,&nbsp;Jurui Yu ,&nbsp;Yilin Zhong ,&nbsp;Honggao Fu ,&nbsp;Xiaokun Zhou ,&nbsp;Wenxiang Yi ,&nbsp;Ling Yuan ,&nbsp;Zhiheng Xu ,&nbsp;Dan Xu","doi":"10.1016/j.nbd.2025.106951","DOIUrl":"10.1016/j.nbd.2025.106951","url":null,"abstract":"<div><div><em>WD repeat domain 62</em> (<em>WDR62</em>) was identified as the second most causative gene of autosomal recessive primary microcephaly (MCPH) frequently associated structural abnormalities such as lissencephaly, polymicrogyria as well as hypoplasia of the corpus callosum, however, underlining mechanism behind these abnormality remains unknown. Here we show that either ablation of WDR62 in neural progenitor cells (NPCs) or post-mitotic neurons both impedes cortical neuronal radial migration in the developing brain. WDR62 modulates the transition from multipolar to bipolar states in migrating neurons and ensures the accurate formation of contralateral projections of callosal neurons. Our results further indicated that ASD-related mutations in WDR62 are associated with a reduced capacity for neuronal migration in the developing brain. Finally, we provide the molecular evidence that the levels of Reelin, a key modulator of neuronal migration and high confidence ASD candidate gene, were significantly reduced in the brains of <em>Wdr62</em> deficient mice. These finding define critical roles for WDR62 in cortical neuronal radial migration and callosal projection which provides insights into the pathogenesis of WDR62 deficiency-related brain dysplasia.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"211 ","pages":"Article 106951"},"PeriodicalIF":5.1,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolomics-driven exploration of sphingosine 1-phosphate mechanisms in refractory epilepsy","authors":"Xinyu Ben ,&nbsp;Chang Li ,&nbsp;Jiaqi Liu ,&nbsp;Ting Liu,&nbsp;Jingyi Tong,&nbsp;Qifu Li","doi":"10.1016/j.nbd.2025.106953","DOIUrl":"10.1016/j.nbd.2025.106953","url":null,"abstract":"<div><div>This study aims to investigate the role of sphingosine 1-phosphate (S1P) in refractory epilepsy (RE) and elucidate its underlying molecular mechanisms. We employed metabolomics technology to analyze serum metabolites and gene expression patterns in individuals with RE. Additional omics analyses were conducted using cellular and animal models to explore the specific functions of S1P and related metabolic pathways. Our findings demonstrated that ACER3/SphK1/S1P play protective roles in maintaining mitochondrial structure and function. These elements were shown to mitigate neuronal hyperexcitability and protect against neuronal damage. By elucidating the dysregulation of metabolic pathways associated with disease onset and progression, our research illuminated the impact of abnormal sphingolipid metabolism and gene expression variances on the manifestation and progression of RE. This research underscores the critical impact of abnormal sphingolipid metabolism on RE development and progression. The insights gained from this study provide a foundation for developing targeted pharmaceutical interventions and symptomatic treatments for individuals with RE.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"212 ","pages":"Article 106953"},"PeriodicalIF":5.1,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compromised retinoic acid receptor beta expression accelerates the onset of motor, cellular and molecular abnormalities in a mouse model of Huntington’s disease","authors":"Nicolas Zinter,&nbsp;Tao Ye,&nbsp;Hanna Semaan,&nbsp;Valérie Fraulob,&nbsp;Damien Plassard,&nbsp;Wojciech Krezel","doi":"10.1016/j.nbd.2025.106943","DOIUrl":"10.1016/j.nbd.2025.106943","url":null,"abstract":"<div><div>The mechanisms underlying detrimental effects of mutant Huntingtin on striatal dysfunction in Huntington’s disease (HD) are not well understood. Although retinoic acid receptor beta (RARβ) emerged recently as one of the top regulators of transcriptionally downregulated genes in the striatum of HD patients and mouse models, its involvement in disease progression remains elusive. Here we challenged functional relevance of RARβ dysregulation in HD onset and progression. Using a series of genetic mouse models, we investigated whether genetically reduced <em>Rarβ</em> expression synergizes with disease- causing mutant huntingtin (mHTT) fragment in R6/1 mice to accelerate HD-like behavioral, cellular and molecular striatal deregulations. We report that genetically compromised <em>Rarβ</em> signaling accelerates onset of motor abnormalities in the R6/1 HD mouse model. Transcriptional profiling revealed that downregulation of <em>Rarβ</em> expression in <em>Rarβ</em>^<em>+/-</em>; R6/1 mice also accelerates transcriptional signature of disease progression and aging by emergence of a cluster of upregulated genes related to cell-cycle, stem cell maintenance and telencephalon development, contributing thereby to degradation of striatal cell-identity. Reactivation of proliferative activity in the neurogenic niche and development-related transcriptional programs in the striatum prompt an attempt of lineage infidelity in HD striatum which may lead as a consequence to disease-driving energy crisis, as suggested by downregulation of oxidative phosphorylation genes, a well-accepted correlate of HD physiopathology, and a metabolic condition required for maintenance of proliferative activity and differentiation but not compatible with high energetic demand of differentiated and active neurons. Overall, our data indicate that RARβ delays disease progression, perhaps by delaying aging process.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"212 ","pages":"Article 106943"},"PeriodicalIF":5.1,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144030190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An analysis of prognostic risk and immunotherapy response of glioblastoma patients based on single-cell landscape and nitrogen metabolism","authors":"Minfeng Tong ,&nbsp;Zhijian Xu ,&nbsp;Lude Wang ,&nbsp;Huahui Chen ,&nbsp;Xing Wan ,&nbsp;Hu Xu ,&nbsp;Song Yang ,&nbsp;Qi Tu","doi":"10.1016/j.nbd.2025.106935","DOIUrl":"10.1016/j.nbd.2025.106935","url":null,"abstract":"<div><div>Glioblastoma (GBM) is a highly invasive brain tumor of astrocytic origin. Nitrogen metabolism plays an instrumental role in the growth and progression of various tumors, including GBM. This study intended to mine nitrogen metabolism-related biomarkers for GBM-related research of prognosis and immunotherapy. Through single-cell data analysis of GBM, we identified four cell types (Astrocytes, Macrophages, Fibroblasts, and Endothelial cells). We calculated the nitrogen metabolism scores and conducted trajectory analysis for the most abundant cells, Astrocytes, revealing 6 differentiation directions of Astrocytes, which included the main differentiation direction from cells with low nitrogen metabolism scores to cells with high nitrogen metabolism scores. Furthermore, based on the differentially expressed genes (DEGs) with high/low nitrogen metabolism scores, we constructed a 7-gene prognostic model by utilizing regression analysis. qRT-PCR analysis showed that IGFBP2, CHPF, CTSZ, UPP1, TCF12, ZBTB20 and RBP1 were all significantly up-regulated in the GBM cells. Through differential analysis, a protein-protein interaction (PPI) network, and enrichment analyses, we identified and analyzed the DEGs in the high RiskScore subgroup, revealing complex interactions among DEGs, which were mainly related to pathways such as TNF signaling pathway and NF-κB signaling pathway. By leveraging univariate analysis, survival-related genes were selected from the nitrogen metabolism-related gene sets. Clustering, survival, immune, and mutation analyses manifested that the collected nitrogen metabolism-related genes had good classification performance, presenting notable differences in survival rates, immune levels, gene mutations, and sensitivity to drugs between cluster1 and cluster2. In conclusion, the project investigated the prognosis and classification value of nitrogen metabolism-related genes in GBM from multiple perspectives, predicting the sensitivity of different subtypes of patients to immunotherapy response and drug sensitivity. These findings are expected to show new research directions for further exploration in these fields.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"211 ","pages":"Article 106935"},"PeriodicalIF":5.1,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143931989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential roles of human tau isoforms in the modulation of inflammation and development of neuropathology","authors":"Brian Spencer,&nbsp;Aaron Schueler,&nbsp;Daniel Sung,&nbsp;Robert A. Rissman","doi":"10.1016/j.nbd.2025.106942","DOIUrl":"10.1016/j.nbd.2025.106942","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is the most common tauopathy characterized by progressive accumulation of Aß and tau neuropathology. Tau is expressed in two major isoforms containing either 3 or 4C-terminal repeats, 3R and 4R. Despite tau isoforms occurring in roughly equimolar ratios in AD, the majority of research focus in developed mouse and <em>in vitro</em> models focus only on 4Rtau. To generate a more complete model of AD tauopathy and understand specific tau isoform-mediated neuropathology and neurodegeneration, we generated a transgenic mouse line expressing both 3Rtau and 4Rtau and determined how this impacted the timing and severity of neuropathological and behavioral changes.</div></div><div><h3>Methods</h3><div>3Rtau-tg and 4Rtau-tg mice were crossed to generate 3R/4Rtau-tg bigenic mice. At 3, 6, and 9 months of age, mice were assessed for behavior, neuropathology and RNA expression.</div></div><div><h3>Results</h3><div>3R/4Rtau bigenic mice expressed increased tau and phosphorylated tau in the hippocampus and cortex compared to single (3R or 4R) transgenic cohorts as early as 3-months of age and this was accompanied with increased astrogliosis and microglial activation. Bigenic mice had significantly greater behavioral deficits compared to either single transgenic littermates in spatial learning and memory as well as nest building, indicative of depression and/or cognitive deficits.</div></div><div><h3>Conclusion</h3><div>This new mouse model of tauopathy more completely recapitulates the pattern, severity and accumulation of tau and associated neuropathology and behavioral changes observed in human tauopathies such as AD. 3R/4Rtau-tg bigenic mice should supplant existing single transgenic tau models for general validation of therapeutic targets and investigations of novel therapies on tauopathy endpoints.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"211 ","pages":"Article 106942"},"PeriodicalIF":5.1,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-linear microglial, inflammatory and oligodendrocyte dynamics across stages of Alzheimer's disease","authors":"Aurélien M. Badina ,&nbsp;Kelly Ceyzériat ,&nbsp;Quentin Amossé ,&nbsp;Alexandre Tresh ,&nbsp;Laurene Abjean ,&nbsp;Léa Guénat ,&nbsp;Emilie Vauthey ,&nbsp;Stergios Tsartsalis ,&nbsp;Philippe Millet ,&nbsp;Benjamin B. Tournier","doi":"10.1016/j.nbd.2025.106950","DOIUrl":"10.1016/j.nbd.2025.106950","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is characterized by cognitive decline and neuropathological hallmarks including Aβ plaques and Tau tangles. Emerging evidence indicates oligodendrocyte (OL) dysfunction and demyelination also contribute to disease progression. Here, we analyzed OL markers and inflammatory gene expression in human hippocampal samples at early and late AD stages. In early AD, we observed OL and myelinating pathways downregulation, alongside microglial and astrocytic activation, as well as upregulated chemokine CCL2 and peripheral immune infiltration markers. In late stages, expression of OL-related genes and myelination pathways increase, with a higher NG2/MBP ratio, coinciding with decreased microglial coverage and peripheral immune markers. These findings indicate that early neuroinflammation may impair OL function, while attenuated immune activity in late AD allows partial OL recovery. This study provides insights into stage-specific inflammatory and myelin-related changes in AD, supporting the relevance of understanding oligodendrocyte dynamics and potential regenerative responses for future therapeutic strategies.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"211 ","pages":"Article 106950"},"PeriodicalIF":5.1,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycosylation in neurodevelopment: What oncology teaches?","authors":"Hours Camille ,&nbsp;Gressens Pierre","doi":"10.1016/j.nbd.2025.106945","DOIUrl":"10.1016/j.nbd.2025.106945","url":null,"abstract":"<div><div>Neurodevelopment is a highly complex process, sensitive to a multitude of signaling pathways linked to molecular processes involved in neuronal development and function, metabolism, and immune functions. Key pathways include cell-cycle regulation (PI3K/Akt/mTOR, p53/PTEN), JAK-STAT, Notch, SLIT/Robo, epithelial-mesenchymal transition (EMT) and cellular homeostasis processes such as apoptosis, autophagy and hypoxia. Transcription regulation (including histone and epigenetic regulation) and immune regulation (NF-kB, Toll-like receptors (TLRs)) play a crucial role. Glycosylation abnormalities related to these molecular processes have been described in cancer. However, while cancer research and therapies have been revolutionized by the study of glycosylation, mechanistic insights and therapeutic approaches are still struggling to develop in neurodevelopmental pathologies. This study is a blueprint to unravel the key pathological pathways in neurodevelopment by highlighting the benefits of studying the associated regulatory processes of glycosylation, which have led to major advances in cancer research.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"211 ","pages":"Article 106945"},"PeriodicalIF":5.1,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}