Journal of Molecular Neuroscience最新文献

{"title":"Advancements in the Study of Missense Mutations in ABCA7 in Alzheimer’s Disease","authors":"Lixin Liu,&nbsp;Bin Zhu","doi":"10.1007/s12031-026-02526-9","DOIUrl":"10.1007/s12031-026-02526-9","url":null,"abstract":"<div>\u0000 \u0000 <p>Alzheimer’s disease (AD) is a neurodegenerative disorder affecting millions of people worldwide. In recent years, genetic factors, particularly missense mutations in susceptibility genes, have been proven to play a key role in the pathogenesis of AD. The <i>ABCA7</i>, a regulator of lipid metabolism and amyloid-beta clearance, has missense mutations that impact phospholipid transport and phagocytic functions, thus contributing to the development of AD. Genome-wide association studies (GWAS) and whole-genome sequencing have identified various missense mutations in <i>ABCA7</i>, such as G1527A and R880Q, with risk ratios up to 1.15 times. Furthermore, differences in the distribution of these mutations across different ethnic groups have been widely reported. Future research should focus on the prevalence and functional effects of these mutations in different populations and their specific effects on <i>ABCA7</i> protein function. A deeper understanding of these mutations could provide new scientific bases for the early diagnosis and treatment of AD. In summary, the missense mutations in <i>ABCA7</i> provide important insights into the genetic susceptibility of AD and represent potential candidate targets for the development of personalized treatment strategies.</p>\u0000 </div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147737856","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":"Nicotinic Acetylcholine Receptor of α7 Subtype is Linked to Glioblastoma Cholinergic Heterogeneity","authors":"Elena Gondarenko,&nbsp;Diana Mazur,&nbsp;Andrei Siniavin,&nbsp;Polina Arkhangelskaya,&nbsp;Valery Maiorov,&nbsp;Igor Ivanov,&nbsp;Igor Kasheverov,&nbsp;Nadine Antipova,&nbsp;Irina Shelukhina,&nbsp;Denis Kudryavtsev","doi":"10.1007/s12031-026-02523-y","DOIUrl":"10.1007/s12031-026-02523-y","url":null,"abstract":"<div>\u0000 \u0000 <p>Glioblastoma multiforme (GBM) shows tremendous heterogeneity in terms of morphology and gene expression. One of the diagnostically significant characteristics of GBM is the choline peak that can be found in patients’ NMR. Choline derivatives are distributed unevenly throughout the tumor and concentrated, in particular, at the leading edge and infiltrating GBM tumour zones as well as gene transcripts of α7 nicotinic acetylcholine receptor (nAChR), known for its ability to become activated upon choline binding. Since agonist-induced nAChR up-regulation in brain and cell lines has been described and several studies have highlighted the role of nAChR ligands in glioblastoma proliferation in vivo, here we hypothesize for the first time that the complex architecture of glioblastoma might develop partially through choline activation of calcium-permeable α7 nAChR that may contribute to changes in gene expression networks. Using the U87MG glioblastoma cell line, we demonstrated that selective α7 nAChR ligands – agonist (PNU282987) and positive allosteric modulator (PNU120596), and antagonist of α7 and α9 nAChRs (α-cobratoxin, α-CTX, from <i>Naja naja</i> venom) – dynamically regulate nAChR subunit mRNA expression (CHRNA4, CHRNA5, CHRNA6, CHRNA7, CHRNA9). α-CTX suppressed agonist-induced CHRNA7 up-regulation in U87MG cells and increased cell viability. Proteomic analysis revealed altered expression of cytoskeletal (ACTG1), metabolic (SHMT2, GLRX3), and endoplasmic reticulum-associated (GANAB) proteins, suggesting the involvement of calcium-dependent signaling downstream of α7 nAChR activation. Quantitative PCR, proteomics and cell viability data were integrated by cellular automata model imitating glioblastoma growth and exposed details of tumour progression, which supports a role for α7 nAChR as one of multiple factors that can help shape intratumoural heterogeneity. These results may have implications for the development of personalized treatment strategies. However, since these findings were obtained in a single cell line, further validation in additional GBM models and in vivo systems is needed before broader conclusions can be drawn.</p>\u0000 </div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147738275","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":"Temporal Biomarker Profiles Following Non-Surgical Spinal Cord Concussion","authors":"Taylor M. Dickson,&nbsp;Anastasiya Loos,&nbsp;Malaika Amin,&nbsp;Juliana Vivas Lopez,&nbsp;Susan F. Murphy,&nbsp;Pamela J. VandeVord,&nbsp;Kelly C. S. Roballo","doi":"10.1007/s12031-026-02520-1","DOIUrl":"10.1007/s12031-026-02520-1","url":null,"abstract":"<div>\u0000 \u0000 <p>Traumatic spinal cord concussion (SCC) can result from motor vehicle accidents, contact sports, falls, and other mild traumatic events. Although clinically significant, the relationship between SCC severity and long‑term outcomes remains unclear. Identifying biochemical biomarkers that reflect post‑injury physiological and molecular changes may improve assessment and guide therapeutic decisions. Similar to advances in traumatic brain injury, integrating biomarkers with imaging and behavioral evaluations could enhance SCC characterization. This study examined biomarkers linked to neuroinflammation and repair mechanisms, ubiquitin C‑terminal hydrolase L1 (UCH‑L1), nitric oxide (NO), glial fibrillary acidic protein (GFAP), and brain‑derived neurotrophic factor (BDNF), and characterized their temporal profiles in a preclinical SCC model. Male Sprague–Dawley rats were assigned to either a blast‑induced SCC group or a sham group. Animals were euthanized at 24 h, 72 h, or 6 weeks post‑injury for spinal cord culture preparation and blood collection. UCH‑L1 and other neuronal injury markers remained elevated from the acute through chronic phases in spinal cord cultures and ex vivo serum, indicating neuronal damage. NO displayed a biphasic pattern with an early increase at 24 h, a decrease at 72 h, and renewed elevation at six weeks, suggestive of inflammatory and oxidative stress responses. GFAP levels rose progressively across all time points, consistent with glial activation. In contrast, BDNF levels showed minimal change, suggesting limited neurotrophic support after SCC. Overall, these biomarker expressions on the SCC cell culture and ex vivo serum indicate an ongoing neuronal stress, chronic inflammation, and glial reactivity. UCH‑L1 appears particularly promising for detecting and monitoring SCC‑related injury, while NO and GFAP offers complementary insight into inflammatory response. Combined with clinical assessments, these biomarkers may improve injury stratification and prediction of long‑term outcomes.</p>\u0000 </div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697555","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":"Integrated Transcriptomics and Machine Learning Reveal Lipid Metabolism Related Genes in Ischemic Stroke","authors":"Qiu-Lin Wang,&nbsp;Chang-Le Fang,&nbsp;Tian-Hao Bao,&nbsp;Rui-Ze Niu","doi":"10.1007/s12031-026-02519-8","DOIUrl":"10.1007/s12031-026-02519-8","url":null,"abstract":"<div>\u0000 \u0000 <p>Lipid metabolism dysregulation is considered a key metabolic feature of ischemic stroke (IS) and may also contribute to its related neuropsychiatric complications. However, its critical regulatory molecules remain unclear. By integrating machine learning methods with transcriptomic analyses, this study systematically characterized the molecular networks underlying lipid metabolism in IS. Using bulk RNA-seq data obtained from the middle cerebral artery occlusion model, we observed a significant increase in lipid metabolic activity. By combining differential gene expression analysis, Weighted Gene Co-expression Network Analysis, and machine learning algorithms, we ultimately identified Hmox1, Stat3, and Tlr2 as core genes associated with lipid metabolism dysregulation. Functional enrichment analysis highlighted the strong association between these genes and lipid metabolism pathways. Further single-cell transcriptomic analyses emphasized the significant role of MG in the lipid metabolism disorder of IS. Furthermore, differential gene expression, functional enrichment analysis, and virtual knockout indicated that Hmox1, Stat3 and Tlr2 in microglia were closely related to lipid metabolic activity. In summary, this study identified Hmox1, Stat3, and Tlr2 as potential regulatory targets for microglial lipid metabolism in IS, providing a novel theoretical foundation for understanding the IS mechanism and its potential neuropsychiatric complications and for developing targeted intervention.</p>\u0000 </div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147687683","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":"Clinical Study on the Combined Use of Tadalafil and Epalrestat in the Treatment of Diabetic Neurovascular Erectile Dysfunction","authors":"Peng Sun,&nbsp;Miao Yu","doi":"10.1007/s12031-026-02504-1","DOIUrl":"10.1007/s12031-026-02504-1","url":null,"abstract":"<div>\u0000 \u0000 <p>This study aims to evaluate the clinical efficacy of tadalafil combined with epalrestat in the treatment of diabetic neurovascular erectile dysfunction (ED). Eighty patients diagnosed with diabetic neurovascular ED admitted to between January 2022 and October 2024 were randomly allocated into two groups (<i>n</i> = 40 each). The control group received tadalafil monotherapy, while the observation group was additionally treated with epalrestat. Both regimens lasted 12 weeks. Outcomes assessed pre- and post-treatment included International Index of Erectile Function-5 (IIEF-5), Erection Hardness Score (EHS), modified Sexual Life Quality Questionnaire (mSLQQ-QoL), penile hemodynamic parameters [peak systolic velocity (PSV), end-diastolic velocity (EDV), resistance index (RI)], and serum markers of endothelial function [endothelin-1 (ET-1), von Willebrand factor (vWF), and asymmetric dimethylarginine (ADMA)]. Treatment safety was also evaluated. Post-treatment, both groups showed significant improvements in IIEF-5 scores, proportion of EHS grade III-IV, and mSLQQ-QoL scores, with greater changes observed in the combination group (<i>P</i> &lt; 0.05). The combination group also demonstrated higher PSV and RI, and lower EDV, ET-1, vWF, and ADMA levels than the control group (<i>P</i> &lt; 0.05). No drug-related adverse events occurred in either group (<i>P</i> &gt; 0.05). Tadalafil combined with epalrestat therapy for diabetic neurovascular ED can synergistically improve erectile function, erection hardness, sexual life quality, penile hemodynamics, and vascular endothelial function, with good safety and no increased risk of drug-related adverse events.</p>\u0000 </div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147642584","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":"Akira Arimura Foundation Akira Arimura Foundation 2027–2028 Young Investigator Grant Application Procedures","authors":"","doi":"10.1007/s12031-026-02517-w","DOIUrl":"10.1007/s12031-026-02517-w","url":null,"abstract":"","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147621427","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":"Striatal Dysregulation of Angpt2 and Circadian Gene Expression in a Rotenone Rat Model of Parkinson’s Disease","authors":"Dalia Y Al Saeedy,&nbsp;Elisa Hawkins,&nbsp;Mikhail G Dozmorov,&nbsp;Ohm Tripathi,&nbsp;Sina Mahdiani,&nbsp;Fay M Jahr,&nbsp;Ola AlAzzeh,&nbsp;Laxmikant S. Deshpande,&nbsp;Joseph L. McClay","doi":"10.1007/s12031-026-02506-z","DOIUrl":"10.1007/s12031-026-02506-z","url":null,"abstract":"<div>\u0000 \u0000 <p>Rotenone is a naturally-occurring isoflavone that is used as a pesticide. Rotenone is also administered to rats to induce nigrostriatal dopaminergic neuron loss in an established model of Parkinson’s Disease (PD). However, the molecular mechanisms linking rotenone action to the emergence of PD-like phenotypes are poorly understood. Here, we characterize rotenone-induced gene dysregulation in the striatum. Male Lewis rats at 12–14 months received rotenone injected at 3 mg/kg, i.p. once daily for nine days. Behavioral effects of rotenone were verified using the bar test for catalepsy. RNA sequencing was carried out on RNA extracted from the striatum of rats receiving the full course of Rotenone treatment and vehicle-treated controls. Illumina PE150 sequencing to 30 M clusters per sample revealed several hundred differentially expressed genes (DEGs) at FDR &lt; 5%. These included Dopa decarboxylase (<i>Ddc</i>), which encodes an important enzyme in dopamine production, and Angiopoietin 2 (<i>Angpt2</i>), a gene previously implicated in analysis of post-mortem PD brain. Pathway analysis of top findings identified the Circadian Clock System as enriched with rotenone DEGs. Circadian and sleep dysfunction is a known feature of PD. We validated the differential expression of two circadian genes via quantitative PCR: downregulation of Period 3 (<i>Per3</i>) and upregulation of the aryl hydrocarbon receptor nuclear translocator-like (<i>Arntl</i>). Overall this study represents a first look at striatal dysregulation of gene expression in the established rotenone PD model and indicates that further study of circadian gene dysregulation in this model may be fruitful.</p>\u0000 </div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12031-026-02506-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589317","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":"A Bioinformatic Analysis of BAG Protein Interactors and Pathways in Alzheimer’s and Parkinson’s Disease","authors":"Sudarshan Ramanan,&nbsp;Gail V. W. Johnson","doi":"10.1007/s12031-026-02514-z","DOIUrl":"10.1007/s12031-026-02514-z","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative disorders. Within the scope of neurodegenerative disorders, the Bcl-2 associated athanogene (BAG) family proteins and associated interactors have been a key area of focus. The BAG family is a group of proteins that contain at least one evolutionarily conserved BAG domain. Despite this similarity, their interactions and functions can vary widely. So far, research has predominantly scrutinized individual BAG proteins, rather than explore potential cooperative actions among family members. Some BAG family members may function together thereby indicating potential interactions within this family. Although connections among BAG members have been observed, their role in neurodegenerative disorders, such as AD and PD, remains largely uncharacterized. This mini review explores the common pathways, intersections, and differences within these interactions as well as their link to AD and PD. Using computational techniques to mine transcriptomic data, several groupings of pathways that these BAG family members are involved in were identified in the context of AD and PD. Understanding these pathways and their relationships may uncover potential gaps in current research and help identify novel therapeutic targets for the treatment of these neurodegenerative diseases.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589310","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":"Circ-find-0001774 Modulates Parkinson’s Disease via miR-153-3p: Mechanistic Insights and Therapeutic Implications","authors":"Ronglan Zhu,&nbsp;Jie Chen,&nbsp;Tao Song,&nbsp;Yun Yang,&nbsp;Chaoyang Zhou,&nbsp;Zhiping Xie,&nbsp;Min Yuan,&nbsp;Jianzhong Zhang","doi":"10.1007/s12031-026-02509-w","DOIUrl":"10.1007/s12031-026-02509-w","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to investigate how circ-find-0001774 regulates miR-153-3p in Parkinson’s disease (PD).</p><h3>Methods</h3><p>We first validated the targeting relationship between circ-find-0001774 and miR-153-3p using dual-luciferase reporter assays, excluding any association with let-7a-5p. Next, we constructed a circ-find-0001774 overexpression vector and transfected it into MN9D dopaminergic neurons, confirming transfection efficiency by qPCR. In vitro, we induced a PD cell model with 100 µmol/L MPP+ iodide for 24 h and assessed cell proliferation using CCK-8, apoptosis via flow cytometry, and miR-153-3p and LC3Ⅱ/Ⅰ protein levels by qPCR and Western blotting. In vivo, we established a mouse PD model by daily intraperitoneal injection of 18 mg/kg MPTP for seven days, evaluating motor function through behavioral tests, observing brain pathology via HE staining, and analyzing miR-153-3p and β-catenin protein levels by qPCR and Western blotting.</p><h3>Results</h3><p>Dual-luciferase assays confirmed a specific targeting interaction between miR-153-3p and circ-find-0001774. In vitro, circ-find-0001774 overexpression significantly enhanced cell proliferation, reduced apoptosis and decreased miR-153-3p and LC3Ⅱ/Ⅰ protein expression levels. In vivo, circ-find-0001774 overexpression notably ameliorated motor deficits in the mouse PD model mitigated neurodegeneration, decreased miR-153-3p level and increased β-catenin protein expression levels.</p><h3>Conclusion</h3><p>Our study reveals that circ-find-0001774 modulates miR-153-3p, mainly through the Wnt/β-Catenin signaling pathway, suggesting its therapeutic potential for PD. These findings provide novel insights and experimental foundations for further developing PD treatment strategies.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147571573","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":"Docosahexaenoic Acid Modulates Autophagy and Confers Neuronal Resilience under Hypoxia–Reoxygenation Stress","authors":"Francis Zamora,&nbsp;Manuel L. Montero,&nbsp;Jo-Wen Liu,&nbsp;Viet Hoang Dinh,&nbsp;Johnny D. Figueroa,&nbsp;Marino A. De León","doi":"10.1007/s12031-026-02512-1","DOIUrl":"10.1007/s12031-026-02512-1","url":null,"abstract":"<div>\u0000 \u0000 <p>Hypoxia dramatically worsens neuronal death after injuries and strokes, as neurons rely heavily on oxidative phosphorylation for energy. This study investigated the effects of docosahexaenoic acid (DHA) in reducing cell death in nerve cells. Neuron-like cells, nerve growth factor-differentiated PC12 (NGFDPC12) cell cultures, with or without DHA pretreatment, were exposed to hypoxic conditions (0.5% O₂) for 12 to 48 h, followed by reoxygenation. Results showed that hypoxia caused a significant increase in the stress-response gene HIF-1α, with mRNA levels rising 5.47- and 6-fold at 24 and 48 h, respectively, compared to normoxic controls. Similarly, the pro-apoptotic gene BNIP3 was elevated 3.37- and 2.9-fold at the same time points. After 24 h of hypoxia, cells showed significant reactive oxygen species (ROS) buildup and displayed apoptotic features. The expression of fatty acid-binding protein 5 (FABP5), which is involved in responding to oxidative stress, also increased under hypoxic conditions. Treatment with DHA or rapamycin significantly improved cell viability after hypoxic exposure. To determine whether DHA protects by activating autophagy, we measured the expression of critical autophagy-related genes Atg5, Atg7, and Atg12. Hypoxia suppressed Atg5 and Atg7 expression; however, DHA restored and markedly increased the levels of Atg5, Atg7, and Atg12 beyond those in normoxic conditions. Immunoblot analysis supported these findings, showing higher levels of phosphorylated Beclin-1 and conjugated LC3, two key autophagy markers. These findings support our prior research, suggesting that DHA’s neuroprotective effects during hypoxia may involve the activation of autophagy pathways, highlighting its potential as a therapeutic strategy.</p>\u0000 <p><b>Impact Statement</b></p>\u0000 <p>This study reveals that docosahexaenoic acid (DHA), an omega-3 fatty acid abundant in the brain, enhances neuronal resilience to hypoxia–reoxygenation injury by restoring autophagy function and limiting oxidative stress. These findings uncover a previously underappreciated role for DHA as a modulator of redox-sensitive autophagy pathways and suggest potential therapeutic strategies for ischemic and metabolic neurodegenerative disorders.</p>\u0000 </div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"76 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147571614","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}