Molecular Neurobiology最新文献

{"title":"Maladaptive Neuroplasticity Under Stress: Insights into Neuronal and Synaptic Changes in the Prefrontal Cortex.","authors":"Bingyu Ren, Quan Yuan, Shuhan Cha, Sinyi Liu, Jifeng Zhang, Guoqing Guo","doi":"10.1007/s12035-025-05152-5","DOIUrl":"10.1007/s12035-025-05152-5","url":null,"abstract":"<p><p>Chronic stress can lead to maladaptive neuroplastic changes in the brain, with the prefrontal cortex (PFC) being a critical site of vulnerability due to its role in executive function and emotional regulation. Extensive evidence has confirmed that chronic stress induces neuroplasticity changes at multiple scales, including functional reorganization, intrinsic neuronal excitability, and structural and synaptic plasticity. These alterations are particularly prominent in glutamatergic pyramidal neurons of the PFC and involve synaptic weakening, dendritic retraction, spine loss, and impaired long-term potentiation. The paradoxical findings regarding pyramidal neuron excitability-ranging from hyper- to hypoactivity-highlight the complex and dynamic nature of stress-induced plasticity. One proposed mechanism linking these alterations is excitotoxicity, characterized by excessive glutamate signaling, impaired astrocytic clearance, and calcium overload, ultimately leading to synaptic dysfunction and structural degeneration. Additionally, inhibitory interneurons and glial cells might also play essential roles in shaping and modulating the stress response. This review integrates findings across neuroplasticity levels to provide a comprehensive understanding of how chronic stress reshapes the PFC. We further discuss the therapeutic potential of targeting homeostatic plasticity as a compensatory mechanism and propose future directions to clarify temporal dynamics, circuit specificity, and molecular regulators underlying maladaptive neuroplasticity in stress-related disorders.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"15227-15249"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144369074","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":"Integrative Single-Cell Analysis Decodes Gene Expression and Chromatin Accessibility in the Developing Human Fetal Brain.","authors":"Tiantian Xu, Huihui Tao, Lingling Zhou, Haiyan Yu, Shi Bai, Hui Guo, Zhipeng Zeng, Wei Shi, Chunmei Wen, Mengyao Wu, Xuejia Zheng, Pingping Ye, Yuan Fang, Mingquan Guo, Donge Tang, Yong Dai","doi":"10.1007/s12035-025-05184-x","DOIUrl":"10.1007/s12035-025-05184-x","url":null,"abstract":"<p><p>The brain is the core of the central nervous system, responsible for regulating and integrating various physiological and psychological functions. Abnormal disruptions in genes during brain development can lead to a range of neurodevelopmental disorders. In this study, we performed a systematic investigation of human fetal brain tissue from miscarriages between 8 and 17 weeks of gestation using integrated single-cell RNA sequencing (scRNA-seq) and single-cell transposase-accessible chromatin sequencing (scATAC-seq). We constructed single-cell transcriptomic and epigenomic maps of neurodevelopment, revealing key signaling pathways involved in neural cell proliferation, differentiation, and functional maturation. Through pseudotime analysis, we reconstructed the developmental trajectory of neuronal differentiation and its dynamic regulatory mechanisms. Additionally, we identified cell type-specific chromatin accessibility regions during neurogenesis and, through integrated analysis, predicted potential regulatory elements involved in the process. Overall, the single-cell multi-omics integration map constructed in this study provides valuable resources for a deeper understanding of fetal brain development, cellular heterogeneity, lineage relationships, and transcriptional regulatory networks during neurogenesis.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"14101-14120"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637668","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":"Targeting of the PI3 K/AKT/GSK3β Pathway in Parkinson's Disease: A Therapeutic Blueprint.","authors":"Raed AlRuwaili, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Ali K Albuhadily, Athanasios Alexiou, Marios Papadakis, Mohammed E Abo-El Fetoh, Gaber El-Saber Batiha","doi":"10.1007/s12035-025-05113-y","DOIUrl":"10.1007/s12035-025-05113-y","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a neurodegenerative disease characterized by progressive motor and non-motor symptoms. PD neuropathology is due to the progressive deposition of mutant alpha-synuclein (α-Syn) in the dopaminergic neurons of the substantia nigra pars compacta (SNpc). This effect initiates oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis of the dopaminergic neurons in the SNpc. PD neuropathology, which is closely associated with inflammatory and oxidative disorders, disrupts different vital cellular pathways. Notably, the current anti-PD medications only relieve the symptoms of PD without averting the underlying neuropathology. Thus, it is advisable to search for novel drugs that attenuate the progression of PD neuropathology. It has been shown that phosphatidylinositol 3-kinase (PI3K), AKT, and glycogen synthase kinase 3 beta (GSK3β) signaling pathways are affected in PD. PI3K/AKT pathway is neuroprotective against the development and progression of PD. However, the over-activated GSK3β signaling pathway has a detrimental effect on PD neuropathology by inducing inflammation and oxidative stress. Dysregulation of the PI3K/AKT/GSK3β signaling pathway provokes brain insulin resistance (BIR), neuroinflammation, and neuronal apoptosis, the hallmarks of PD and other neurodegenerative diseases. However, the mechanistic role of the PI3K/AKT/GSK3β signaling pathway is not fully clarified. Therefore, in this review, we intend to discuss the role of the PI3K/AKT/GSK3β signaling pathway in PD pathogenesis and how PI3K/AKT activators and GSK3β inhibitors have helped effectively manage PD.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"15108-15131"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pinocembrin Alleviates Postoperative Cognitive Dysfunction in Aged Mice by Modulating miR-384-5p/FZD1 Axis to Activate the Wnt/β-Catenin Pathway.","authors":"Jie Li, Xue-Li Peng, Xin-Yu Cheng, Jun-Jun Yang, Cui Cui, Jian-Hui Liu","doi":"10.1007/s12035-025-05181-0","DOIUrl":"10.1007/s12035-025-05181-0","url":null,"abstract":"<p><p>Postoperative cognitive dysfunction (POCD) is a clinically recognized complication of surgery that compromises long-term neurological outcomes, though its mechanistic basis remains poorly defined. The flavonoid Pinocembrin (5,7-dihydroxyflavanone) exhibits anti-inflammatory, antioxidant, and neuroprotective effects. However, the precise mechanisms underlying Pinocembrin's role in modulating the pathogenesis and progression of POCD remain incompletely elucidated. Cognitive function was evaluated using the Morris water maze (MWM) test and open field test (OFT). Protein and mRNA expression levels were quantified by Western blotting and qRT-PCR, respectively. Neuronal apoptosis in hippocampal tissue was assessed using TUNEL staining, while BV-2 microglial apoptosis was analyzed by flow cytometry. Microglial activation was visualized via immunofluorescence staining. Pro-inflammatory cytokine concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Pinocembrin significantly improved cognitive function in elderly POCD mice, without altering locomotor activity or anxiety-like behaviors. Notably, Pinocembrin reduced neuronal apoptosis and microglia-induced inflammation in elderly POCD mice. Mechanistically, Pinocembrin attenuated BV-2 microglial apoptosis and M1 polarization by downregulating miR-384-5p. MiR-384-5p directly targets FZD1. Strikingly, Pinocembrin rescued FZD1 expression by downregulating miR-384-5p, while FZD1 knockdown abolished Pinocembrin's effects on microglial M1 polarization and apoptosis. This cascade activated the Wnt/β-catenin pathway, ultimately ameliorating cognitive deficits in POCD mice. Pinocembrin ameliorates POCD in aged mice by activating Wnt/β-catenin signaling via the miR-384-5p/FZD1 regulatory axis.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"13975-13988"},"PeriodicalIF":4.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584313","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":"Retraction Note: Combination Therapy of Mesenchymal Stem Cell Transplantation and Astrocyte Ablation Improve Remyelination in a Cuprizone-Induced Demyelination Mouse Model.","authors":"Soheila Madadi, Elham Shiri, Parichehr Pasbakhsh, Fatemeh Tahmasebi, Shokoofeh Kazemzadeh, Kazem Zibara, Iraj Ragerdi Kashani","doi":"10.1007/s12035-025-05275-9","DOIUrl":"https://doi.org/10.1007/s12035-025-05275-9","url":null,"abstract":"","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275210","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":"The Impact of Maternal Obesity and Deprivation On Energy Metabolism, Oxidative Stress and Brain Antioxidant Defense in the Neurodevelopment of Offspring in the Short, Medium and Long Term.","authors":"Mariella Reinol Steiner, Aline Haas de Mello, Daniele Hendler Salla, Catarina Barbosa Chaves Bressan, Rayane Luiz Mendes, Mariana Pacheco de Oliveira, Larissa Espindola da Silva, Bruna Barros Fernandes, Igor Ramos Lima, Rubya Pereira Zaccaron, Gislaine Zilli Réus, Paulo Cesar Lock Silveira, Emílio Luiz Streck, Gislaine Tezza Rezin","doi":"10.1007/s12035-025-05070-6","DOIUrl":"10.1007/s12035-025-05070-6","url":null,"abstract":"<p><p>The current global obesity epidemic is often associated with changes in dietary habits and lifestyle. Increasing evidence from both observational and experimental animal studies has highlighted the relationship between prenatal exposures and an increased predisposition to metabolic and cognitive disorders, as well as obesity in adulthood. In this study, we used a rodent model to investigate brain energy metabolism by assessing mitochondrial respiratory chain complexes I and II, along with oxidative stress markers (DCF) and antioxidant defenses (GSH and SOD), aiming to identify potential alterations in the central nervous system during offspring neurodevelopment. Our results demonstrated increased body weight and mesenteric fat accumulation in early life and adolescence, along with an imbalance in brain energy metabolism when maternal obesity and early-life stress (maternal deprivation) were combined. By exploring the complex interactions between gestational exposures and long-term behavioral and metabolic outcomes in an experimental model, our findings contribute to a better understanding of the developmental origins of health and disease.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"12473-12487"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136333","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":"Protein Structure-based FUS Mutational Subtypes Are Associated With Protein Mislocalization in Amyotrophic Lateral Sclerosis Patients.","authors":"Wanli Yang, Zhen Luo, Xuelin Tang, Jingyan Guo, Xi Chen, Yi Dong, Yi-Min Sun, Dongsheng Fan, Ke Xu, Yan Chen, Ming Zhang","doi":"10.1007/s12035-025-05085-z","DOIUrl":"10.1007/s12035-025-05085-z","url":null,"abstract":"<p><p>The mislocalization of RNA-binding proteins (RBPs) from nucleus to cytoplasm and the formation of aggregates are hallmarks of neurodegeneration. Amyotrophic lateral sclerosis (ALS) disease-causing mutations in the fused in sarcoma (FUS) gene, encoding an RNA-binding protein, cluster at the C-terminal proline/tyrosine-nuclear localization signal (PY-NLS) domain, which is crucial for mediating nucleus-cytoplasm translocation by binding to Transportin-1. However, the mechanisms underlying heterogeneous protein mislocalization and age at onset (AAO) of ALS cases carrying FUS PY-NLS mutations remain unclear. Here, we screened FUS mutations in 416 ALS patients, and identified 12 patients carrying four FUS mutations at the p.R521 locus of PY-NLS domain (p.R521P, p.R521C, p.R521G, p.R521H), exhibiting highly variable AAO (20-56 years). AlphaFold-2 predicted protein structures classified FUS p.R521 mutants into alpha-helix containing (p.R521C, p.R521H) and alpha-helix disrupted (p.R521P, p.R521G) subgroups. Isothermal titration calorimetry experiment showed that the FUS alpha-helix disrupted subgroup had a reduced binding affinity with transportin-1, which is essential for mediating the nucleus-cytoplasm translocation. Furthermore, immunofluorescence in HEK-293 T and SH-SY5Y cells revealed more protein mislocalization in the FUS alpha-helix disrupted subgroup compared to the alpha-helix containing subgroup. FUS mislocalization status is also significantly associated with ALS AAO. Finally, the alpha-helix structure based FUS-ALS subgroups exhibited significantly different AAO (P = 0.036) in our cohort, but not in a Chinese cohort including published dataset. In summary, we showed highly diverse phenotypes in ALS patients with FUS R521 mutants, and implicated a link between genetic mutation related C-terminal structure with the status of FUS protein mislocalization.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"12461-12472"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143097","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":"LncRNA SNHG14 Regulates the Expression of BDNF by Recruiting Histone Methyltransferase EZH2 to Mediate H3K27me3, Thereby Affecting Angiogenesis and Functional Recovery After Cerebral Ischemia.","authors":"Tao Ding, Li Zhang","doi":"10.1007/s12035-025-05021-1","DOIUrl":"10.1007/s12035-025-05021-1","url":null,"abstract":"<p><p>We aimed to probe the role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14) on angiogenesis and functional recovery after cerebral ischemia (CI) by recruiting histone methyltransferase enhancer zeste homolog 2 (EZH2) to mediate trimethylation of lysine 27 on histone H3 (H3K27me3) and thus modulate brain-derived neurotrophic factor (BDNF) expression. The Zea Longa method was employed to establish a rat model of right middle cerebral artery occlusion (MCAO). Longa method was applied to assess the neurological deficits in rats; ELISA was adopted to test the levels of inflammatory factors (interleukin (IL)-1β, IL-6, and IL-8) in the cortical tissue of the ischemic penumbra; HE staining and TUNEL staining were implemented to observe the pathological changes and apoptosis in the ischemic penumbra cortex; and immunohistochemistry staining was implemented to observe the CD34 positive expression level and microvascular density (MVD) in the ischemic penumbra cortex. The expression levels of SNHG14, EZH2, and BDNF in the cortical tissue of the ischemic penumbra were determined by RT-qPCR or WB, and the interactions among KCNQ1OT1, EZH2, and TIMP-3 were verified by RNA-pull down, RIP, and ChIP experiments. Increased levels of SNHG14 and EZH2 were observed in the cortical tissue of the ischemic penumbra in MCAO rats, accompanied by decreased BDNF levels. Both downregulation of SNHG14 and downregulation of EZH2 ameliorated neurological deficits in CI rats, reduced the level of inflammatory factors and apoptosis, alleviated damage to the cortical tissue of the ischemic penumbra, and increased MVD. Upregulation of EZH2 or downregulation of BDNF reversed the improvement effects of SNHG14 downregulation on neurological function and angiogenesis in CI rats. Mechanistically, SNHG14 could mediate H3K27me3 and thus inhibit BDNF expression by recruiting EZH2. Downregulation of SNHG14 ameliorates neurological function and angiogenesis in CI rats through the EZH2/BDNF axis.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"12511-12522"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151258","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":"Late-Stage Activation of Toll-like receptor 3 Alleviates Cognitive Impairment and Neuropathology in an Alzheimer's Disease Mouse Model.","authors":"Taiyang Zhu, Fanyu Shen, Xiao Jia, Hui Zhou, Wanyan Ni, Shang Wang, Di Wu, Huimin Gao, Zhenying Shang, Yan Zhou, Jingjing Han, Guoliang Jin, Fuxing Dong, Jie Zu, Xinxin Yang, Hongjuan Shi, Chao Zhou, Fang Hua","doi":"10.1007/s12035-025-05092-0","DOIUrl":"10.1007/s12035-025-05092-0","url":null,"abstract":"<p><p>This study was to investigate the effects of Toll-like receptor-3 (TLR3) activation on cognitive impairment and neuropathology in late-stage of Alzheimer's disease in a mouse model. Amyloid protein precursor (APP)/presenilin-1 (PSEN1) (APP/PSEN1) mice were treated with Poly (I:C), a specific for TLR3. A panel of neurobehavioral tests were conducted to evaluate their cognitive functions. Aβ deposition, plasma Aβ levels, neuropathological changes, and activation of TLR3- TIR-domain-containing adapter-inducing interferon-β (TRIF) signaling were assessed by magnetic resonance imaging (MRI), electrophysiological recordings, transmission electron microscopy, Western blotting, immunofluorescence staining, and qPCR. The data demonstrated that Poly (I:C) significantly attenuated cognitive and neuropathological impairments, compared with APP/PSEN1 mice without Poly (I:C) treatment. Administration of Poly (I:C) significantly reduced brain Aβ_1-42 deposition and the levels of Aβ_1-40 and Aβ_1-42 in peripheral blood. In addition, treatment with Poly (I:C) significantly up-regulated the expression of anti-inflammatory factors and inhibited the expression of pro-inflammatory factors. The data indicated that systemic application of TLR3 agonist Poly(I:C) attenuated the brain damage, improved the cognitive function, and reduced the levels of Aβ_1-42 in brain and peripheral blood. The underlying mechanism might attribute to the up-regulation of p-IRF3 that increases the expression of anti-inflammatory factors and the inhibition of p-NF-κB that reduces the expression of pro-inflammatory factors.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"12616-12633"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12433446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling Moxibustion's Impact on AD Mice Learning and Memory: Role of Mitochondrial Respiratory Chain Complex I Subunit in the Hippocampus.","authors":"Yuan Shen, Hong-Ying Li, Qing-Qing Yang, Ke Zhang, Shu-Qing Liu, Ning Zhang, Chen-Yu Li, Shu-Guang Yu, Lu-Shuang Xie, Qiao-Feng Wu","doi":"10.1007/s12035-025-05147-2","DOIUrl":"10.1007/s12035-025-05147-2","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by significant impairment in energy metabolism. Our previous studies have demonstrated that moxibustion can ameliorate cognitive dysfunction by enhancing brain energy metabolism in individuals with AD, yet its fundamental mechanism remains incompletely understood. In this study, spatial transcriptomics, biochemical assays, and transmission electron microscopy were utilized to identify differentially expressed genes related to metabolism and their functions, as well as to determine the key metabolic genes influenced by moxibustion. Moxibustion significantly promote spatial learning and memory ability, while reducing the production of hippocampal pathological markers in APP/PS1 mice. Respiratory chain complex I may play an important role in regulating energy metabolism in the hippocampus during moxibustion. Additionally, moxibustion also elevated co-expression of PSD95/SYN, which exhibited a positive correlation with energy metabolism. Thus moxibustion has the potential to improve energy metabolism and synaptic plasticity in the hippocampus, subsequently ameliorating learning and memory impairments.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"13413-13429"},"PeriodicalIF":4.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144326291","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}