Journal of Neurochemistry最新文献

{"title":"Cerebrospinal Fluid sCD27 as a Biomarker of Neuroinflammatory Disease: A Systematic Review and Meta-Analysis.","authors":"Nadia Damholt Savino, Malene Bredahl Hansen, Amanda Marie Lund Christiansen, Sahla El Mahdaoui, Finn Sellebjerg, Jeppe Romme Christensen","doi":"10.1111/jnc.70451","DOIUrl":"https://doi.org/10.1111/jnc.70451","url":null,"abstract":"<p><p>Neuroinflammatory diseases of the central nervous system (CNS) present considerable diagnostic challenges due to overlapping clinical features and the lack of specific biomarkers capable of reliably detecting CNS inflammation. Soluble CD27 (sCD27) is a marker of adaptive immune activation, released upon CD27-CD70 interaction. sCD27 has emerged as a promising cerebrospinal fluid (CSF) biomarker, but its clinical utility remains unclear. This systematic review and meta-analysis aimed to clarify the diagnostic value of CSF sCD27 across neuroinflammatory conditions. We systematically searched PubMed, Embase, and Scopus for studies reporting CSF sCD27 levels in neuroinflammatory disorders versus controls, including demyelinating diseases, autoimmune encephalitis, neuroinfectious diseases, and primary CNS lymphoma, following PRISMA 2020 guidelines. Nineteen studies met the inclusion criteria for qualitative synthesis, and ten provided sufficient quantitative data for meta-analysis, encompassing 685 neuroinflammatory and 751 control participants. Using multivariate and random-effects models, we found significantly elevated levels of CSF sCD27 in neuroinflammatory diseases compared to controls (standardized mean difference [SMD] = 1.24, 95% CI 0.98-1.51, p < 0.0001), with consistent results in sensitivity and subgroup analysis restricted to multiple sclerosis. Despite between-study heterogeneity, largely driven by variation in assay methods, reporting units, and study populations, effect sizes remained large and robust. Most studies also reported excellent diagnostic accuracy, with area under the curve (AUC) values above 0.85, supporting the discriminatory potential of CSF sCD27 for neuroinflammatory diseases versus controls. Collectively, these findings strongly support that CSF sCD27 is a robust biomarker of adaptive immune-mediated neuroinflammation across a spectrum of neuroinflammatory diseases. Future research should focus on assay standardization and consistent reporting practices using well-characterized prospective cohorts of a broader spectrum of neuroinflammatory disorders to define clinical thresholds and facilitate the integration of CSF sCD27 into diagnostic protocols. This study provides a comprehensive synthesis and substantiates CSF sCD27 as a promising biomarker for detecting adaptive immune-mediated neuroinflammation in clinical practice.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 5","pages":"e70451"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13123749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydroxytyrosol Mitigates Anxiety-Like Behaviors After a Traumatic Experience in Aged Mice in Parallel With Increased Neurogenesis in the Ventral and Dorsal Dentate Gyrus, and Preservation of Gut Microbiota Composition.","authors":"Giorgio D'Andrea, Laura Bertini, Marco Costanzi, Fabiana Canini, Roberta Bernini, Andrea Fochetti, Mariangela Clemente, Silvia Proietti, Manuela Ceccarelli, Carla Caruso, Maurizia Caruso, Ferdinando Scavizzi, Marcello Raspa, Felice Tirone, Laura Micheli","doi":"10.1111/jnc.70448","DOIUrl":"10.1111/jnc.70448","url":null,"abstract":"<p><p>Hydroxytyrosol (HTyr), a phenolic compound present in olive oil, exhibits antioxidant, anti-inflammatory, and neuroprotective properties, benefiting several age-related diseases. Our previous research demonstrated that oral HTyr administration counteracts age-associated neurogenesis decline in the dentate gyrus of the hippocampus by promoting the production of stem/progenitor cells and new neurons. Since new neurons generated in the dorsal dentate gyrus support contextual memory discrimination, while those generated in the ventral region modulate anxiety, we investigated whether pure HTyr, synthesized in our laboratories, selectively stimulates neurogenesis in these regions in aging mice and evaluated its effects on contextual memory and stress response. Furthermore, we examined its influence on gut microbiota composition, given the well-established role of the microbiota-gut-brain axis in memory and stress regulation. We found that HTyr induced the production of new neurons and neuroblasts in both dentate gyrus regions, with a prevalent effect in the ventral region. Consistently, we observed that HTyr treatment did not improve the contextual memory discrimination but reduced fear sensitization and anxiety-like behavior after a traumatic experience. Furthermore, we observed a reduction of neuroinflammation in HTyr-treated dentate gyri. In parallel, treatment with HTyr preserved the stability of key microbial families linked to intestinal well-being, counteracting the unhealthy effects of stress on gut microbial structure. Our results suggest that HTyr treatment in aging mice enhances resilience to posttraumatic stress by increasing neurogenesis and modulating the microbiota-gut-brain axis. Future studies should explore its potential as a therapeutic intervention for individuals experiencing posttraumatic stress disorder symptoms.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 5","pages":"e70448"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13131041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chromaffin Versus Platelet Granules: What We Have Learned From Chromaffin Cells for Human Studies.","authors":"Ricardo Borges","doi":"10.1111/jnc.70433","DOIUrl":"https://doi.org/10.1111/jnc.70433","url":null,"abstract":"<p><p>Biological amines-such as dopamine, norepinephrine, epinephrine, octopamine, serotonin, and histamine-are stored at high concentrations within secretory vesicles, also referred to as \"granules\" in certain cell types, including mast cells, chromaffin cells, and platelets. Over the past decades, extensive knowledge has been gained regarding the biogenesis, composition, and function of chromaffin granules. This information can now be leveraged to understand amine storage mechanisms in other secretory systems, particularly in human platelets, which are readily accessible. Importantly, dysfunction of secretory vesicles has been implicated in several diseases, and vesicular defects may therefore be detectable in platelets obtained from well-characterized individuals. Such an approach offers significant potential for clinical and translational studies, as personalized functional information can be directly derived from patients. In this brief review, I focus on the vesicular mechanisms involved in biological amine accumulation and discuss the functional consequences of their disruption, with particular emphasis on chromaffin granules and platelet δ-granules.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 5","pages":"e70433"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"Targeting Glutamate Excitotoxicity with Memantine Modulates Glial Response and Protects Motoneurons After Spinal Root Lesion\".","authors":"","doi":"10.1111/jnc.70453","DOIUrl":"https://doi.org/10.1111/jnc.70453","url":null,"abstract":"","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 5","pages":"e70453"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urine-Derived iPSC Neurospheres Uncover Proteomic Correlates of Clinical Severity in Dravet Syndrome.","authors":"Michele Martins, Guillaume Nugue, Andrey Aguiar, Leticia R Q Souza, Paulo V Abrantes, Julia Rodrigues Trajano, Mariana Stelling, Magno Junqueira, Stevens Rehen, Marília Zaluar P Guimarães","doi":"10.1111/jnc.70452","DOIUrl":"10.1111/jnc.70452","url":null,"abstract":"<p><p>Dravet syndrome (DS) is a rare and severe childhood-onset developmental epileptic encephalopathy caused primarily by mutations in the sodium channel gene SCN1A. Animal models have undeniably advanced our understanding of DS, but they still do not fully capture its clinical heterogeneity, highlighting the need for complementary human in vitro systems. Here, we generated induced pluripotent stem cells (iPSCs) from urine epithelial cells of three DS patients carrying distinct SCN1A variants and differentiated them into neural stem cells (NSCs) and early-stage neurospheres. Clinical severity was assessed using the DANCE checklist, and molecular phenotypes were characterized through isobaric quantitative proteomics. Comparative analyses identified differences in protein abundance across patient-derived lines, with distinct molecular patterns associated with clinical severity measures. The patient-derived lines exhibited variability in protein groups related to synaptic organization, mitochondrial processes, and RNA processing, reflecting interindividual molecular differences within the cohort. These findings establish patient-derived neurospheres as a scalable human model for investigating molecular variability in DS. This approach provides a framework to explore disease heterogeneity and provides a foundation for future studies linking molecular profiles to clinical variability in DS.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 5","pages":"e70452"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating Sphingomyelins Correlate With Plasma T-Tau in Cognitively Unimpaired Older Adults at Risk of Developing Alzheimer's Disease.","authors":"Tahmida Sharmin, James D Doecke, Pratishtha Chatterjee, Steve Pedrini, Hamid R Sohrabi, Nicholas J Ashton, Henrik Zetterberg, Manohar L Garg, Kaj Blennow, Ralph N Martins","doi":"10.1111/jnc.70436","DOIUrl":"https://doi.org/10.1111/jnc.70436","url":null,"abstract":"<p><p>Alterations in plasma sphingomyelin (SM) levels have been reported in Alzheimer's disease (AD), pointing to disturbances in lipid metabolism that may contribute to disease pathogenesis. Neuronal damage in early AD triggers tau release into central and peripheral systems. Despite influence from peripheral contributions, alterations in plasma total-tau (T-tau) remain valuable in indicating AD-related neurodegeneration. Investigating relationships between SM metabolism and tau release during preclinical AD may uncover important biochemical processes and support advancing early non-invasive detection and treatment approaches. This cross-sectional study investigated cognitively unimpaired (CU) older adults from the KARVIAH cohort, grouped by cortical amyloid-β (Aβ) status through positron emission tomography (PET) imaging (CU Aβ- and CU Aβ+) and utilised a Biocrates-targeted metabolomic platform and Single-molecule array (Simoa) technology to quantify plasma levels of SMs and T-tau, respectively. Associations between circulating SMs and T-tau were examined within each group, with T-tau-associated SMs further evaluated for their association with cognitive performance and cortical Aβ burden and their potential to discriminate CU Aβ+ from CU Aβ- individuals. Significant positive correlations were observed between SMs and T-tau levels exclusively in CU Aβ+ individuals, suggesting connections between SM-mediated biochemical pathways and tau release from early neurodegeneration in preclinical AD. Lower SM levels were associated with weaker working memory and executive function, as well as poorer global cognition, indicating their potential predictive value for weaker cognitive performance. Moreover, SMs were also inversely associated with cortical Aβ load in CU Aβ+ individuals, possibly reflecting early SM-mediated neuroprotective responses against AD pathogenesis. Receiver operating characteristic analysis further revealed the significant potential of the SM panel in distinguishing cortical PET-Aβ status and enhancing the predictive performance of plasma T-tau in CU individuals. Therefore, circulating T-tau-associated SMs may serve as promising early biomarkers of lipid-mediated processes in CU older adults with cortical amyloid pathology and tau-related neurodegeneration.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 5","pages":"e70436"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When Pathways Converge: Iron, Lipid Peroxidation, and α-Synuclein in Ferroptosis-Driven Dopaminergic Neurodegeneration","authors":"Carmem L. Sperlich,&nbsp;Brent R. Stockwell,&nbsp;Marcelo Farina","doi":"10.1111/jnc.70438","DOIUrl":"10.1111/jnc.70438","url":null,"abstract":"<p>The selective degeneration of dopaminergic neurons is a hallmark of Parkinson's disease and related disorders. While multiple cell death pathways have been implicated, ferroptosis has recently emerged as a critical mechanism. This iron-dependent form of regulated cell death is driven by the accumulation of phospholipid hydroperoxides, leading to oxidative membrane damage. Dopaminergic neurons are intrinsically vulnerable to ferroptosis due to their high iron content, active dopamine metabolism (a source of reactive oxygen species), and relatively low antioxidant defenses. Here we synthesize evidence linking ferroptosis to dopaminergic neurodegeneration in Parkinson's disease and related conditions, detailing the molecular mechanisms involving iron dyshomeostasis, lipid peroxidation, and α-synuclein pathology. We further evaluate growing preclinical data demonstrating that pharmacological inhibition of ferroptosis is neuroprotective and discuss the clinical implications, therapeutic potential, and ongoing challenges of translating these findings into effective treatments for patients.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 4","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70438","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147674436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Effects of Poly(I:C)-induced Neuroinflammation on Hippocampal Astrocyte Function and Glycolytic Metabolism","authors":"Adriana Fernanda K. Vizuete,&nbsp;João Pedro Montandon Garcez,&nbsp;Maria Cristina M. Pellenz,&nbsp;Jordana Agliardi de Lima,&nbsp;Jéssica Taday,&nbsp;Jéssica Maria Souza,&nbsp;Marina Concli Leite,&nbsp;Carlos Alberto Gonçalves","doi":"10.1111/jnc.70434","DOIUrl":"10.1111/jnc.70434","url":null,"abstract":"<div>\u0000 \u0000 <p>Concern is growing about the role of neurotropic viruses, such as Zika virus, West Nile virus, herpes simplex virus, SARS-CoV-2, and human immunodeficiency virus, in central nervous system (CNS) infections, which trigger host immune responses, neuronal dysfunction and brain injury. Astrocytes function as immune system cells and, together with microglia, participate in the activation and maintenance of neuroinflammatory responses, a common pathophysiological event in neurodegenerative diseases. The reactive phenotype of glial cells leads to the synthesis and release of inflammatory mediators inducing a neurometabolic shift to nonoxidative glycolysis, a phenomenon similar to the Warburg effect. However, since viruses require energy from host cells to replicate, it is essential to understand the increase in glucose consumption during viral infections. For this purpose, we used an early polyinosinic:polycytidylic acid [Poly(I:C)] induced neuroinflammation model to investigate its effects on astrocyte function and neurometabolic responses in two approaches: acute hippocampal slices and in vivo intraperitoneal administration from male <i>Wistar</i> rats (PN30). We evaluated the effects of a dose–response curve of Poly(I:C), an immunostimulant agent that mimics double-stranded RNA virus infection, on the neuroinflammatory response, astrocyte reactivity, and glycolytic parameters. Poly(I:C) induced neuroinflammation and astrocyte reactivity in a dose-dependent manner. Both models of Poly(I:C)-induced early neuroinflammation and astrocyte reactivity which leads to neurometabolic reprogramming with enhanced several glycolytic parameters, such as glucose uptake and hexokinase activity, methylglyoxal (MG) synthesis and affect the glyoxalase-1 (GLO1) activity. Accordingly, inflammatory and glycolytic inhibitors reduced the glycolytic parameters induced by Poly(I:C). As expected, the inflammatory inhibitors downmodulated neuroinflammatory parameters, with arundic acid in particular reversing astrocyte reactivity. Moreover, the downregulation of the glycolytic pathway had a greater effect on the pronounced inflammatory process, and reversed the astrocyte reactivity induced by Poly(I:C) neuroinflammation. Our data are consistent with the hypothesis that a metabolic shift is required to maintain neuroinflammatory signaling, particularly in early Poly(I:C) induced neroinflammation, and highlight the glycolytic pathway as a potential target for controlling the neuroinflammatory response.</p>\u0000 <p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 4","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147674381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Astrocyte Bioenergetic Remodeling as a Central Trait of Disrupted Glucocorticoid Signaling: Mechanisms and Implications for Stress Vulnerability”","authors":"","doi":"10.1111/jnc.70439","DOIUrl":"10.1111/jnc.70439","url":null,"abstract":"<p>Hanus, P., D. Frydecka, and M. Ślęzak. 2026. “Astrocyte Bioenergetic Remodeling as a Central Trait of Disrupted Glucocorticoid Signaling: Mechanisms and Implications for Stress Vulnerability.” <i>Journal of Neurochemistry</i> 170, no. 3: e70394. https://doi.org/10.1111/jnc.70394.</p><p>In the paper by Hanus et al. (2026), affiliation 1 was incorrectly given as Medical University of Wrocław. This has been corrected to Wrocław Medical University.</p><p>We apologize for this error.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 4","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70439","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATG14-Mediated SNARE Complex Activation Promotes ΔFosB Degradation to Ameliorate Levodopa-Induced Dyskinesia","authors":"Yi Wu,&nbsp;Ke Liu,&nbsp;Zhaoyuan Zhang,&nbsp;Zhuoran Ma,&nbsp;Zhicheng Tang,&nbsp;An Chang,&nbsp;Haoxuan Ouyang,&nbsp;Heng Zhai,&nbsp;Xuebing Cao,&nbsp;Yan Xu","doi":"10.1111/jnc.70431","DOIUrl":"10.1111/jnc.70431","url":null,"abstract":"<p>The chronic accumulation of ΔFosB in striatal medium spiny neurons has been implicated as a pivotal contributor to the pathogenesis of levodopa-induced dyskinesia (LID). While recent studies have implicated autophagy in the degradation of ΔFosB and the amelioration of LID, the precise mechanisms remain elusive. We induced LID in a unilateral 6-hydroxydopamine-lesioned parkinsonism rat model via chronic levodopa treatment. To modulate the autophagy pathway, we overexpressed ATG14 in the striatum of LID rats and administered chloroquine, an autophagy inhibitor, peripherally. We assessed LID severity using abnormal involuntary movements (AIMs) scores. Western blotting, real-time quantitative polymerase chain reaction, immunofluorescence, immunohistochemistry, transmission electron microscopy, and Golgi staining were employed to measure autophagy flux, synaptic alterations, and ΔFosB levels. Chronic levodopa treatment reduced ATG14 and SNARE complex (STX17, SNAP29, and VAMP8) levels, disrupted their interaction, impaired autophagy flux, affected synaptic function, and led to ΔFosB accumulation in the striatum of PD rats. Upregulating ATG14 in the striatum of LID rats improved AIMs scores, facilitated SNARE-mediated autophagosome-lysosome fusion, restored synaptic deficits, and promoted ΔFosB degradation. However, these beneficial effects of ATG14 upregulation were negated by chloroquine administration. Our findings suggest that upregulating ATG14 enhances SNARE formation, promoting autophagy flux and thereby reducing LID occurrence by facilitating ΔFosB degradation.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 4","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13063209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}