Neuroscience最新文献

{"title":"Neuromodulation of resting state brain network topography by heterolateral prefrontal transcranial photobiomodulation","authors":"Licong Li ,&nbsp;Zhaoning Du ,&nbsp;Kun Wang ,&nbsp;Xuexiu Li ,&nbsp;Fukuan Zhang ,&nbsp;Guanghai Zhang ,&nbsp;Peng Xiong ,&nbsp;Xiuling Liu","doi":"10.1016/j.neuroscience.2026.02.012","DOIUrl":"10.1016/j.neuroscience.2026.02.012","url":null,"abstract":"<div><div>This study aims to explore the distinct effects of left and right prefrontal Transcranial Photobiomodulation (tPBM) on brain functional networks and to quantify the neuromodulation responses of functional brain networks constructed from EEG data under stimulation from heterolateral targets. 18 healthy, young, right-handed participants with no history of neuropsychological disorders participated in two tPBM sessions over a 3-week period. Resting-state EEG data were collected before and after tPBM. Functional connectivity, measured by coherence, and graph theory analysis (GTA) were applied to delta, theta, alpha, and beta bands to assess both global and local network topology. 810 nm tPBM targeting the right prefrontal cortex significantly enhanced long-range functional connectivity in the delta, theta, and beta bands. It increased the global clustering coefficient in the delta band and decreased it in the alpha band. In contrast, left prefrontal tPBM mainly influenced theta band connectivity, increasing the global clustering coefficient in the delta band and reducing nodal clustering in the right central region in the theta band and the right temporal region in the beta band.</div><div>The findings reveal that both left and right prefrontal 810 nm tPBM induce significant neurophysiological changes in brain network topology. However, the neuromodulation effects differ across brain functional connectivity, as well as global and local network topology levels. The findings in this study provide novel insights into the effects of heterolateral target tPBM stimulation on the brain network and suggest that left prefrontal tPBM could be a potential choice for personalized treatment of neuropsychiatric disorders.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"601 ","pages":"Pages 1-13"},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146195380","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":"Parietal repetitive transcranial magnetic stimulation enhances functional connectivity in patients with minimally conscious state","authors":"Xiao Yan ,&nbsp;Zilong Zhu ,&nbsp;Jubao Du ,&nbsp;Lei Cao ,&nbsp;Xiaoping Wan ,&nbsp;Yanhua Li ,&nbsp;Jiawen Jiang ,&nbsp;Weiqun Song ,&nbsp;Ye Zhang","doi":"10.1016/j.neuroscience.2026.02.020","DOIUrl":"10.1016/j.neuroscience.2026.02.020","url":null,"abstract":"<div><div>The basis of disorders of consciousness is the destruction of brain functional connectivity, and the restoration of damaged connectivity is considered as an indicator of consciousness recovery. The purpose of this study is to explore the effect of parietal repetitive transcranial magnetic stimulation (rTMS) on the changes of brain functional connectivity and consciousness recovery in patients with minimal conscious state (MCS) by electrophysiological (EEG) functional connectivity analysis, and to further explore the potential mechanism of consciousness recovery. In this study, 24 patients with MCS were randomly assigned to either real or sham rTMS group. The real rTMS group was applied to the parietal cortex at 10 Hz with 90% of the rest motor threshold, while the sham group underwent a similar procedure without cortical stimulation. Resting-state EEG and Coma Recovery Scale-Revised (CRS-R) scores were obtained before and after treatment. The Phase Locking Value (PLV) was calculated for the region of interest to assess the effect of parietal rTMS on functional brain connectivity. The CRS-R scores significantly improved after treatment in the real rTMS group, accompanied by increases in PLV, the default mode network (DMN), the frontoparietal network (FPN), and FPN-DMN connectivity. In contrast, the sham rTMS group showed no significant changes in CRS-R scores or EEG results. Moreover, alterations in FPN networks were positively correlated with changes in CRS-R scores. Parietal rTMS promotes the recovery of consciousness by fortifying large-scale brain connections and activating neural networks. In particular, FPN functional connections are closely linked to the early recovery of consciousness.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"601 ","pages":"Pages 29-36"},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147276784","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":"Integrative analysis of spontaneous brain activity in Parkinson’s disease: associations with gene expression, cell types, and receptor density","authors":"Zhan-Xiang Hu ,&nbsp;Yuan-Zhi He ,&nbsp;Xin Huang ,&nbsp;Zhi Wen","doi":"10.1016/j.neuroscience.2026.02.043","DOIUrl":"10.1016/j.neuroscience.2026.02.043","url":null,"abstract":"<div><h3>Background</h3><div>Parkinson’s disease (PD) shows widespread alterations in intrinsic brain activity, yet the molecular and cellular bases of these disruptions remain unclear. Resting-state fMRI metrics—amplitude of low-frequency fluctuations (ALFF) and regional homogeneity (ReHo)—offer complementary views of spontaneous neural activity but have rarely been examined within an integrated biological framework.</div></div><div><h3>Methods</h3><div>We studied 31 PD patients and 28 healthy controls using voxel-wise ALFF and ReHo analyses combined with cortical transcriptomic data from the Allen Human Brain Atlas, cell type–specific gene expression, and PET-derived neurotransmitter receptor density maps. Partial least squares regression identified gene expression patterns associated with PD-related imaging alterations. Enrichment analyses, cell type overlap, and spatial correlations with neurotransmitter receptor distributions were subsequently performed.</div></div><div><h3>Results</h3><div>PD patients showed decreased ALFF in the left putamen, precentral gyrus, and middle frontal gyrus, and decreased ReHo in the left thalamus and cerebellum. ALFF alterations corresponded to negatively loaded PLS1 genes enriched for immune and neuroinflammatory pathways, predominantly expressed in microglia, astrocytes, oligodendrocytes, and endothelial cells. ReHo changes corresponded to positively loaded PLS2 genes enriched for receptor-mediated signaling and transcriptional regulation, mainly expressed by astrocytes. Both ALFF and ReHo patterns showed strong spatial coupling with 5HT2a receptor density, suggesting serotonergic involvement.</div></div><div><h3>Conclusion</h3><div>This multimodal analysis links PD-related ALFF and ReHo alterations to distinct yet converging transcriptomic, cellular, and neurochemical substrates. The findings suggest that PD-related functional alterations spatially align with glial–neurovascular transcriptional gradients and serotonergic receptor distribution, providing convergent but indirect evidence for their involvement in PD-related network reorganization.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"601 ","pages":"Pages 69-82"},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147317887","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":"The antiaging protein Klotho is a key factor in susceptibility to cerebral ischemia","authors":"Penélope Aguilera ,&nbsp;Arturo Hernández-Cruz ,&nbsp;Javier Franco-Pérez ,&nbsp;Irlanda Peralta-Arrieta ,&nbsp;Ivan Alquisiras-Burgos","doi":"10.1016/j.neuroscience.2026.03.005","DOIUrl":"10.1016/j.neuroscience.2026.03.005","url":null,"abstract":"<div><div>Ischemic cerebrovascular events are among the leading causes of death and disability worldwide, disproportionately affecting the elderly due to vascular aging, oxidative stress, and chronic inflammation. During cerebral ischemia, oxygen and glucose deprivation trigger a cascade of pathological events, including excitotoxicity, mitochondrial dysfunction, blood–brain barrier disruption, and neuroinflammation. Emerging evidence identifies Klotho as a multifunctional protein with anti-aging, antioxidant, and anti-inflammatory properties that may confer neuroprotection against ischemic injury. Aging is associated with a progressive decline in Klotho expression, correlating with increased stroke susceptibility and poorer recovery outcomes. Experimental studies demonstrate that Klotho attenuates glutamatergic excitotoxicity by regulating the GluN2B subunit and excitatory amino acid transporters. It reduces oxidative stress through inhibition of NADPH oxidase and activation of SOD2 and FOXO3 pathways, while preserving blood–brain barrier integrity by downregulating aquaporin-4 and matrix metalloproteinase-9. Moreover, Klotho suppresses pro-inflammatory signaling by inhibiting NF-κB, RelA, and NLRP3 inflammasome activation, and enhances anti-inflammatory responses via PPAR-γ modulation. Beyond limiting neuronal death, Klotho promotes neurogenesis and synaptic plasticity by regulating neurotrophic factors and Wnt signaling, thereby supporting neural stem cell survival and functional recovery after ischemia. Collectively, these findings position Klotho as a central regulator of neuronal homeostasis and post-ischemic repair. This review provides the first comprehensive mechanistic integration of Klotho’s neuroprotective role in ischemic cerebrovascular injury, proposing it as a unifying molecular axis linking brain aging to ischemic vulnerability and regenerative capacity.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"601 ","pages":"Pages 136-147"},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147378051","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":"Unravelling the therapeutic potential of chrysin against ischemic stroke and post-stroke cognitive impairment: a network pharmacology and in-silico perspective","authors":"Pooja Gandharvachari Achar ,&nbsp;Kamsagara Linganna Krishna ,&nbsp;Kavana C P ,&nbsp;Mayuri Patil ,&nbsp;Prabitha Prabhakaran ,&nbsp;Chandan Shivamallu ,&nbsp;Chandan Dharmashekar ,&nbsp;Ganavi Bethanagere Ramesha","doi":"10.1016/j.neuroscience.2026.02.007","DOIUrl":"10.1016/j.neuroscience.2026.02.007","url":null,"abstract":"<div><div>Ischemic stroke (IS) is a cerebrovascular disorder that, if left untreated, can lead to secondary neurodegeneration and Post Stroke Cognitive Impairment (PSCI). Current therapies offer a narrow time window, highlighting the need for alternative approaches. Flavonoids, known for their neuroprotective properties, are promising candidates. Chrysin, a flavone with multiple pharmacological activities, was investigated for its therapeutic role in IS and PSCI. Pharmacokinetic and toxicological profiles were assessed using Schrodinger and ProTox III. Target screening was performed via Swiss Target Prediction-STITCH for chrysin and Gene Cards-OMIM for disease targets. Protein-Protein Interaction (PPI), Gene Ontology (GO), and KEGG pathway analyses were conducted using STRING and DAVID. Network construction was done in Cytoscape 3.10.3. Density Functional Theory (DFT) calculations used Schrodinger Jaguar to assess molecular reactivity. Molecular docking and Molecular dynamics simulation studies were also performed using Schrodinger. Chrysin was associated with 134 targets, while IS and PSCI had 3024 and 7472 targets, respectively, with 109 overlapping targets. GO and KEGG analyses showed chrysin’s influence on key cell growth and apoptosis pathways. DFT analysis indicated a HOMO-LUMO energy gap of 0.164342 Hartree, suggesting high reactivity and potential for electron transfer. Docking studies revealed strong binding affinity of chrysin to SIRT1 (−5.108 kcal/mol) and PGC1α (−9.072 kcal/mol). Molecular dynamics confirmed chrysin’s stable interaction, particularly with SIRT1. Chrysin demonstrates potential as a therapeutic agent for IS and PSCI by modulating cellular longevity, oxidative stress, and apoptosis pathways, including MAPK and FoxO signaling.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"599 ","pages":"Pages 14-28"},"PeriodicalIF":2.8,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146193148","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":"The gut-brain axis in diabetic neuropathy, cognitive impairment, and emotional disorders","authors":"Xiao Yu ,&nbsp;Kexin Zhang ,&nbsp;Chengxia Kan ,&nbsp;Yujie Ma ,&nbsp;Sufang Sheng ,&nbsp;Tianpeng Zheng ,&nbsp;Xiaodong Sun","doi":"10.1016/j.neuroscience.2026.02.006","DOIUrl":"10.1016/j.neuroscience.2026.02.006","url":null,"abstract":"<div><div>Diabetes mellitus has become a global public health challenge, with a steadily rising prevalence that imposes substantial socioeconomic burdens. Over recent years, the gut-brain axis (GBA) has garnered significant attention as a crucial biological framework. GBA denotes the intricate network of bidirectional signaling between the gut and the brain via neuronal, endocrine, and immunological pathways, with the connections among gut bacteria, gut barrier function, and neuroendocrine factors significantly influencing the progression of diabetes mellitus. Studies indicate that disruptions in gut microbiota balance and compromised intestinal barrier integrity are significantly associated with the onset of insulin resistance and diabetes mellitus. Gut flora regulates energy metabolism, insulin sensitivity, and immune responses via the generation of metabolites (e.g., short-chain fatty acids), while impaired gut barrier function can trigger systemic chronic inflammation, which in turn promotes insulin resistance. The GBA also influences appetite, energy balance and insulin secretion through neuroendocrine pathways. Imbalances in the gut microbiota may lead to neuroendocrine dysregulation, thereby accelerating diabetes pathogenesis. New diabetes treatment strategies are being explored based on research on the GBA. Modulation of the intestinal microbiome, restoration of gut barrier integrity, and correction of neuroendocrine dysregulation may offer novel avenues for managing diabetes and its associated complications. In conclusion, revealing the multidimensional pathogenesis of diabetes mellitus from the perspective of the GBA will help to develop more effective therapeutic strategies.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"599 ","pages":"Pages 1-11"},"PeriodicalIF":2.8,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161844","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":"Corrigendum to “The mechanism of hypoxia-inducible factor-1α enhancing the transcriptional activity of transferrin ferroportin 1 and regulating the Nrf2/HO-1 pathway in ferroptosis after cerebral ischemic injury”. [Neuroscience 559 (2024) 26–38]","authors":"Haiqian Yao ,&nbsp;Jianan Tian ,&nbsp;Shi Cheng ,&nbsp;Haitong Dou ,&nbsp;Yulan Zhu","doi":"10.1016/j.neuroscience.2026.01.018","DOIUrl":"10.1016/j.neuroscience.2026.01.018","url":null,"abstract":"","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"599 ","pages":"Pages 12-13"},"PeriodicalIF":2.8,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161845","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":"Corrigendum to “Polyamines signalling pathway: A key player in unveiling the molecular mechanisms underlying Huntington’s disease” [Neuroscience 570 (2025) 213–224]","authors":"Amit Shiwal ,&nbsp;Dhanshree Nibrad ,&nbsp;Manasi Tadas ,&nbsp;Raj Katariya ,&nbsp;Mayur Kale ,&nbsp;Nitu Wankhede ,&nbsp;Nandkishor Kotagale ,&nbsp;Milind Umekar ,&nbsp;Brijesh Taksande","doi":"10.1016/j.neuroscience.2026.01.043","DOIUrl":"10.1016/j.neuroscience.2026.01.043","url":null,"abstract":"","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"598 ","pages":"Page 84"},"PeriodicalIF":2.8,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150149","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":"Identification of an Angiotensin-(1–7)-Producing fusion protein in the brain of transgenic rats Reveals a hypotensive effect mediated through modulation of the GABA–nNOS–NO pathway and highlighting Astrocyte–Neuron crosstalk","authors":"Daniele T Alves ,&nbsp;Bernadette Nickl ,&nbsp;Fatimunnisa Qadri ,&nbsp;Robson AS Santos ,&nbsp;Sergio HS Santos ,&nbsp;Maik Gollasch ,&nbsp;Maria Jose Campagnole-Santos ,&nbsp;Michael Bader","doi":"10.1016/j.neuroscience.2026.01.025","DOIUrl":"10.1016/j.neuroscience.2026.01.025","url":null,"abstract":"<div><div>This study explores the anatomical distribution of Angiotensin-(Ang)-(1–7) fusion protein within the central nervous system of the novel transgenic rat model (TG7371). The Ang-(1–7)/Mas pathway of the renin-angiotensin system (RAS) plays a key role in cardiovascular regulation and influences higher brain functions, including cognition and emotion. TG7371 expresses a transgenic Ang-(1–7)-producing fusion protein which resulted in a hypotensive phenotype. Here, we assessed the expression of Ang-(1–7) fusion mRNA and protein in primary cortical cells from neonates and identified their distribution in the brain of adult rats using qPCR, WB, ISH, and immunolabeling. In neonates, Ang-(1–7) mRNA was mainly found in proliferating cells, whereas in adults, it was primarily identified in GFAP-positive astrocytes. The Ang-(1–7) fusion protein, however, was predominantly found in neurons, including GABAergic interneurons and specific pyramidal cells. High protein levels were particularly noted in cardiovascular control regions like the medulla, as well as in other non-cardiovascular areas. TG7371 displayed twofold increase in brain levels of Ang-(1–7) compared to Ang II vs. Control, which remained unchanged, alongside significant changes in the expression of RAS components and nNOS. These findings indicate that the Ang-(1–7) fusion protein modulates the GABA-nNOS-NO-pathway, contributing to the low blood pressure phenotype of these rats, and promotes a mode of astrocytes-neurons-communication. The widespread expression of the fusion protein in the brain also suggests a potential role in modulating mood, cognition, and neurological disorders. Overall, TG7371 presents a valuable model to explore the long-term cardiovascular and neurobehavioral effects of Ang-(1–7), highlighting promising therapeutic implications and neural crosstalk.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"598 ","pages":"Pages 122-139"},"PeriodicalIF":2.8,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137761","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":"Nose-to-brain axis: mechanistic links between nasal microbiome dysbiosis, neuroinflammation, and brain disorders","authors":"Khiany Mathias ,&nbsp;Fabricia Petronilho ,&nbsp;Lucineia Gainski Danielski","doi":"10.1016/j.neuroscience.2026.01.039","DOIUrl":"10.1016/j.neuroscience.2026.01.039","url":null,"abstract":"<div><div>The nasal microbiome has emerged as a previously underrecognized modulator of neuroinflammation and central nervous system (CNS) homeostasis. Beyond its role in respiratory host defense, this microbial niche is anatomically positioned to directly influence brain physiology through olfactory neuronal pathways, systemic immune signaling, and inter-organ communication within the gut–lung–brain axis. Accumulating evidence indicates that nasal microbiome dysbiosis contributes to blood–brain barrier (BBB) dysfunction, microglial activation, and propagation of neurotoxic protein aggregates, processes implicated in neurodegenerative and psychiatric disorders, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and major depressive disorder. This review synthesizes experimental and clinical studies elucidating key mechanisms by which nasal microbial imbalance may impact CNS pathology, including microbial translocation along olfactory neurons, release of pathogen-associated molecular patterns and inflammatory mediators, extracellular vesicle–mediated signaling, and peripheral immune crosstalk. We further highlight clinical observations linking nasal microbiome signatures with olfactory dysfunction, cognitive decline, and altered inflammatory profiles, particularly in systemic conditions such as sepsis. Despite rapid advances in this field, significant knowledge gaps persist, including the limited availability of longitudinal human cohorts capable of establishing causality, incomplete mechanistic validation in translational models, and insufficient characterization of how environmental exposures and aging reshape the nasal microbiome–brain interface. By integrating current evidence and defining these unmet needs, this review positions the nasal microbiome as a promising source of diagnostic biomarkers and a therapeutic target for modulating neuroinflammation and mitigating neurodegenerative progression.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"598 ","pages":"Pages 19-28"},"PeriodicalIF":2.8,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146096899","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}