NeuroMolecular Medicine最新文献

{"title":"Interferon Regulatory Factor 8 Drives Autoimmune Neuroinflammation in Experimental Autoimmune Encephalomyelitis.","authors":"Haruto Ojika, Kazuo Kunisawa, Moeka Tanabe, Yuki Kon, Koyo Yoshidomi, Yuta Naruoka, Moeka Ogawa, Mayu Kondo, Shoya Takeuchi, Aimi Sugiyama, Hiroyuki Tezuka, Hiroki Doi, Tana, Toshitaka Nabeshima, Akihiro Mouri","doi":"10.1007/s12017-026-08952-7","DOIUrl":"https://doi.org/10.1007/s12017-026-08952-7","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system. The interferon regulatory factor (IRF) family comprises transcription factors that regulate immune responses; however, their roles in MS pathogenesis remain unclear. In this study, we investigated whether IRFs are involved in MS pathology using experimental autoimmune encephalomyelitis (EAE) model mice. Among the IRFs examined, IRF8 expression was significantly increased in the spinal cord of EAE model mice and predominantly localized to myeloid cells. Consistently, patients with MS exhibited significantly increased proportions of IRF8-positive myeloid cells in peripheral blood. Notably, IRF8 knockout mice exhibited complete resistance to EAE induction. The mRNA expression levels of neuroinflammatory mediators, including interleukin IL-1β, IL-6, tumor necrosis factor-α, IL-12b, and nitric oxide synthase 2, were significantly reduced in the spinal cord of IRF8 knockout mice. Collectively, these findings suggest that IRF8 is a critical regulator of autoimmune neuroinflammation, highlighting its potential as a therapeutic target for MS.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149271296","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":"Swimming Exercise Ameliorates Neuropathic Pain and Is Associated with Hippocampal H19, miR-22, and Wnt/β-Catenin Signaling.","authors":"Xuan Su, Hui Liu, Yu-Meng Chen, Man-Xuan Huang, Yi-Li Zheng","doi":"10.1007/s12017-026-08953-6","DOIUrl":"10.1007/s12017-026-08953-6","url":null,"abstract":"<p><p>Physical activity is known to ameliorate neuropathic pain (NP); however, the underlying mechanisms, particularly those involving long non-coding RNAs (lncRNAs) in the hippocampus, remain poorly understood. In this study, we assessed the impact of swimming training on NP in a mouse model of sciatic nerve injury (SNI), with a focus on the lncRNA H19 and its associated signaling pathway. A male C57BL/6 mouse model of SNI was established and randomly divided into five groups: naïve, sham, sham + swim, SNI, and SNI + swim. The swimming groups underwent a 6-week training regimen. Pain thresholds were assessed at multiple time points post-modeling, and hippocampal tissues were collected on day 43 for analysis. Six weeks of swimming training significantly attenuated mechanical hypersensitivity in SNI mice. Compared with the SNI group, swimming training was associated with reduced hippocampal expression of H19, Wnt3a, and β-catenin. Histological analyses using HE and Nissl staining demonstrated improved neuronal morphology and preservation of neuronal structure in the hippocampus following swimming training. In addition, swimming training modulated hippocampal neuroinflammation, as evidenced by decreased levels of IL-6 and TNF-α and increased expression of the IL-10. These findings indicate that swimming training effectively alleviates NP and hippocampal neuroinflammation in SNI mice and is accompanied by coordinated changes in hippocampal H19, miR-22, and Wnt/β-catenin signaling. These associations suggest a potential involvement of H19-related molecular responses in exercise-mediated neuroprotection; however, further mechanistic studies are required to establish causal relationships.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149169629","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":"Sigma-1 Receptor Mitigates Poly-GR-Associated Redox Dysregulation by Restoring NRF2/HO1 Signaling in C9orf72-Associated ALS.","authors":"Chao-Yi Tsai, Hsuan-Cheng Wu, Tsung-Ping Su, Eddie Feng-Ju Weng, Shao-Ming Wang","doi":"10.1007/s12017-026-08951-8","DOIUrl":"10.1007/s12017-026-08951-8","url":null,"abstract":"<p><p>Hexanucleotide GGGGCC repeat expansions in C9orf72 produce arginine-rich dipeptide repeat proteins, including poly-GR and poly-PR, that contribute to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Although poly-GR has been linked to oxidative stress and mitochondrial dysfunction, the mechanisms that determine whether antioxidant defenses are preserved or suppressed in poly-GR-expressing motor neurons remain incompletely understood. Here, we investigated whether Sigma-1 receptor (Sigma-1R) modulates poly-GR-associated redox dysregulation in cellular and mouse models. In NSC34 cells, both EGFP-PR₄₂ and EGFP-GR₅₀ expression reduced NRF2 protein levels. EGFP-GR₅₀ expression was also associated with reduced NRF1 and HO1 levels and increased reactive oxygen species (ROS) accumulation. Sigma-1R overexpression or pharmacological activation with fluvoxamine or PRE084 restored NRF2 and HO1 expression and attenuated both cellular and mitochondrial oxidative stress in EGFP-GR₅₀-expressing cells. Co-treatment with the Sigma-1R antagonist NE100 attenuated the agonist-induced restoration of NRF2 and HO1. Furthermore, the NRF2 inhibitor ML385 attenuated agonist-mediated HO1 restoration, supporting the involvement of NRF2 activity in this downstream response. In an AAV-mediated EGFP-GR₅₀ mouse model, Sigma-1R deficiency was associated with shortened survival, reduced NeuN-positive neuronal counts, and decreased NRF2 immunoreactivity in the brain. Together, these findings identify Sigma-1R as a modulator of poly-GR-associated redox dysregulation and neuronal vulnerability and support further investigation of Sigma-1R modulation as a potential therapeutic strategy for C9orf72-associated ALS.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149168205","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":"Markers and Enrichment Strategies for Brain-Derived Extracellular Vesicles: Current Evidence, Limitations and Future Directions.","authors":"Adhish Mazumder, Shubhankhi Dey, Shruti Gupta, Prasenjit Mitra","doi":"10.1007/s12017-026-08950-9","DOIUrl":"10.1007/s12017-026-08950-9","url":null,"abstract":"<p><p>Brain-derived extracellular vesicles (bdEVs) have gained attention as key mediators of central nervous system communication and as minimally invasive biomarkers for neurological and neuropsychiatric disorders due to their presence in cerebrospinal fluid and peripheral biofluids. Despite this promise, their translational application is constrained by difficulties in selective enrichment and reliable assignment of cellular origin. This review summarizes the progression of bdEV isolation methodologies, from bulk physicochemical approaches to immunoaffinity-based, combinatorial, and single-vesicle-resolved strategies, with an emphasis on marker specificity. Using L1CAM as a representative example, we highlight how peripheral expression, extensive proteolytic cleavage, and dominance of soluble forms undermine its utility as a definitive neuronal EV marker. We further evaluate alternative surface and cargo markers proposed for neuron, astrocyte, microglial, and oligodendrocyte-derived bdEVs, identifying candidates such as ATP1A3, AMPA receptor subunits, GLAST, and AQP4 as more biologically grounded, while noting their limitations. Overall, current evidence indicates that no single marker can reliably define bdEV populations and that marker performance is strongly context dependent. Advancing the field will therefore require brain-restricted marker discovery, multiplexed and orthogonal enrichment strategies, single-vesicle validation, and systematic benchmarking against neural reference datasets to establish bdEVs as robust biomarkers and mechanistic reporters in neurobiology and neurological disease research.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112687","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":"Triangulating the Neuroprotective Mechanisms of Pterostilbene in Hyperhomocysteinemia Induced Cognitive Impairment: Insights from In Silico, Proteomics, and Experimental Validation.","authors":"Bhaskar Jyoti Dutta, Saumya Dwivedi, Shubham Dhiman, Sanjiv Singh","doi":"10.1007/s12017-026-08949-2","DOIUrl":"10.1007/s12017-026-08949-2","url":null,"abstract":"<p><p>Hyperhomocysteinemia (HHcy) is a significant risk factor for cognitive impairment (CI), yet effective therapeutic interventions remain limited. Pterostilbene (PTE), a natural stilbene derivative, possesses antioxidant, anti-inflammatory, and neuroprotective properties; however, its mechanisms of action in HHcy-induced CI remain unclear. This study investigated the molecular basis of PTE-mediated neuroprotection using integrated network pharmacology, proteomics, and experimental validation. Key signaling pathways identified included cAMP/PKA/CREB and TLR4-mediated inflammatory signaling. HHcy was induced in rats by oral L-methionine administration, followed by assessment of cognitive performance, neuronal integrity, mitochondrial function, inflammation, and synaptic plasticity. PTE treatment significantly improved spatial learning, memory retention, and recognition memory while preserving hippocampal cytoarchitecture. Mechanistically, PTE restored mitochondrial biogenesis and function through upregulation of PGC-1α and TFAM, normalization of respiratory chain complex activities, and preservation of mitochondrial ultrastructure. Furthermore, PTE enhanced synaptic plasticity by increasing the expression of PSD95, GAP43, and synaptophysin, activated the cAMP/PKA/CREB signaling pathway, and suppressed neuroinflammation through inhibition of TLR4 signaling. Collectively, these findings demonstrate that PTE ameliorates HHcy-induced cognitive deficits by improving mitochondrial function, promoting synaptic integrity, and modulating neuroprotective and inflammatory pathways, highlighting its potential as a promising therapeutic candidate for HHcy-associated cognitive impairment.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001762","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":"Rebalancing α-Synuclein Clearance: Novel Therapeutic Frontiers in Parkinson's Disease.","authors":"Maryam Jabeen, Huma Hameed, Syed Muhammad Ahmad, Tehreem Mushtaq, Mahtab Ahmad Khan, Anam Hameed","doi":"10.1007/s12017-026-08948-3","DOIUrl":"10.1007/s12017-026-08948-3","url":null,"abstract":"<p><p>Parkinson's disease (PD), the second most common neurodegenerative condition, develops because of abnormal protein misfolding and aggregation of α-synuclein with its subsequent intercellular spread. Such pathological changes lead to disruption of neuronal homeostasis and contribute to neuronal degeneration. During normal conditions, α-synuclein clearance is controlled by different types of lysosomal degradation, namely, macro autophagy, chaperone-mediated autophagy (CMA), micro autophagy, and the ubiquitin-proteasome system. Malfunction of these systems results in increased α-synuclein secretion due to exosome-dependent, direct, and damage-induced mechanisms, which, in turn, promotes enhanced intercellular propagation, inflammation, mitochondrial dysfunction, blood-brain barrier leakage, and neuronal cell death. Although several approaches targeting α-synuclein clearance have shown biological activity in preclinical or early clinical studies, consistent disease-modifying efficacy has not yet been established, owing to challenges including target specificity, blood brain barrier penetration, biological heterogeneity, and the limited sensitivity of clinical endpoints. Recent research indicates that successful treatment is more related to restoring the balance of these two processes than to manipulating one of them.In this review, it is proposed that a systems-level approach can be taken where PD is understood as a disease characterized by the imbalance in proteostasis. Potential treatment modalities include small molecules targeting lysosome function (ambroxol, rapamycin, TFEB activators), CMA enhancers, gene therapy, and antibodies against extracellular α-synuclein. Furthermore, new modalities like molecular glue degraders, allostery-based stabilization of α-synuclein tetramers, engineered decoy particles, and bispecific antibodies represent some other possible routes towards multimodal disease modification.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866026","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":"AMBMP Hydrochloride Reverses STZ-Induced Alzheimer-Type Dementia Associated with Wnt/β-catenin/TLR4 Signaling.","authors":"Palak Kalra, Deepak Chaturvedi, Amit Kumar, Amarjot Kaur Grewal, Heena Khan, Varinder Singh, Thakur Gurjeet Singh, Tanveer Singh, Sheikh F Ahmad, Sabry M Attia","doi":"10.1007/s12017-026-08947-4","DOIUrl":"10.1007/s12017-026-08947-4","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a debilitating neurodegenerative disorder with progressive cognitive decline and neuronal loss. This study investigated the neuroprotective effects of AMBMP Hydrochloride, a Wnt/β-catenin agonist, in a streptozotocin (STZ)-induced mice model of AD, elucidating the interplay between dysregulated Wnt/β-catenin signaling and Toll-Like Receptor 4 (TLR4)-mediated inflammation, with Palmitic acid used as a TLR4 pathway modulator. Mice received bilateral intracerebroventricular (i.c.v.) injections of STZ (3 mg/kg) on Day 1 and Day 3, followed by administration of Donepezil (3 mg/kg)/ AMBMP Hydrochloride (5 mg/kg and 10 mg/kg)/Palmitic acid (TLR4 agonist, 20 mg/kg) via the intraperitoneal (i.p.) route from Day 4 to Day 22. STZ-treated mice exhibited significant cognitive dysfunction, characterized by impaired performance in the Morris Water Maze (MWM) task along with increase in acetylcholinesterase (AChE) activity, oxidative stress (thiobarbituric acid reactive substances; TBARS), neuroinflammation [tumor necrosis factor alpha (TNF-α)/Interleukin-6 (IL-6)/Interleukin-1 beta (IL-1β) and nuclear factor kappa B (NF-κB)] and decreased reduced glutathione (GSH) levels. However, AMBMP Hydrochloride significantly improved behavioral and biochemical alterations possibly through modulation of Wnt/β-catenin signaling and attenuation of TLR4-mediated inflammation. Interestingly, Palmitic acid co-treatment was found to counteract these protective effects, further pointing to a role of TLR4 in the pharmacological effect of AMBMP Hydrochloride. In summary, we confirmed that AMBMP Hydrochloride exhibits potent neuroprotective effects associated with modulating Wnt/β-catenin/TLR4 signaling, offering a promising therapeutic approach against Alzheimer-Type Dementia. Future studies should delve deeper into the molecular mechanisms and translational promise of AMBMP hydrochloride, paving the way for its development as a potential candidate for AD management.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857483","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":"Retraction Note: Thymoquinone and Vitamin C Attenuates Pentylenetetrazole-Induced Seizures Via Activation of GABA_B1 Receptor in Adult Rats Cortex and Hippocampus.","authors":"Ikram Ullah, Haroon Badshah, Muhammad Imran Naseer, Hae Young Lee, Myeong Ok Kim","doi":"10.1007/s12017-026-08946-5","DOIUrl":"https://doi.org/10.1007/s12017-026-08946-5","url":null,"abstract":"","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818865","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":"Semaglutide Alleviates LPS-Induced Cognitive Disorder via O-GlcNAcylation of AKT-mTOR Signaling Pathway Components.","authors":"Qiangwei Liu, Lu Chen, Mengxue Zhang, Zhun Wang, Xiaokun Wang, Ying Dong, Kaiyuan Wang, Changyu Jiang, Yiqing Yin","doi":"10.1007/s12017-026-08945-6","DOIUrl":"10.1007/s12017-026-08945-6","url":null,"abstract":"<p><p>Perioperative neurocognitive disorder (PND) manifests as neurocognitive alterations induced by anesthesia and surgical stress. High-risk factors, including advanced age, obesity, diabetes, and preoperative neurological dysfunction, accelerate PND progression, with neuroinflammation serving as a core pathological mechanism throughout PND pathogenesis. Semaglutide regulates neuroinflammation in patients with diabetes and stroke, yet its role in PND remains undefined.A lipopolysaccharide (LPS)-induced inflammatory neurocognitive impairment mouse model was established via intracerebroventricular injection. Mice were treated with semaglutide alone or combined with the O-GlcNAc transferase inhibitor OSMI-1 and AKT-silencing adeno-associated viruses. Behavioral, biochemical and immunofluorescence assays were performed to evaluate cognitive function and molecular changes. Semaglutide significantly rescued LPS-induced cognitive deficits and restored hippocampal O-GlcNAcylation. Mechanistically, LPS inhibited AKT O-GlcNAc modification and AKT-mTOR pathway activity, facilitated mTOR-gephyrin binding, disrupted GABAAR distribution, aggravated neuronal apoptosis, and impaired synaptic plasticity. Semaglutide reversed these abnormalities by elevating AKT O-GlcNAcylation to activate the AKT-mTOR pathway, which triggered mTOR-gephyrin dissociation, restored synaptic GABAAR localization, attenuated neuronal damage, and rescued synaptic plasticity.Semaglutide ameliorates PND via AKT O-GlcNAcylation-mediated AKT-mTOR activation and subsequent neuroprotective effects.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796090","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":"Celiac Disease and the Nervous System: A Comprehensive Overview of Neurological Manifestations and Underlying Mechanisms.","authors":"Arash Yousefzadeh Eshkoori, Mohadeseh Mahmoudi Ghehsareh, Nastaran Asri, Somayeh Jahani-Sherafat, Mostafa Rezaei Tavirani, Alireza Zali, Masiha Amiri, Amirhosein Monazami, Mohammad Rostami-Nejad","doi":"10.1007/s12017-026-08940-x","DOIUrl":"10.1007/s12017-026-08940-x","url":null,"abstract":"<p><p>Celiac disease (CD) is a chronic immune-mediated enteropathy triggered by gluten ingestion in genetically susceptible individuals. While traditionally associated with gastrointestinal (GI) symptoms, CD is increasingly recognized as a systemic disorder with significant neurological involvement. A growing body of evidence links CD to a broad spectrum of neurological manifestations, including gluten ataxia (GA), peripheral neuropathy (PN), epilepsy, migraine, myoclonic disorders, and cognitive impairment. These symptoms may precede or occur independently of GI symptoms, complicating diagnosis and delaying treatment. The underlying mechanisms are multifactorial, involving autoantibody cross-reactivity, neuroinflammation, increased permeability of the intestinal and blood-brain barrier (BBB), gut dysbiosis, and micronutrient deficiencies. This review synthesizes current insights into the pathophysiological basis of CD-related neurological disorders. We also explore the therapeutic impact of a strict gluten-free diet (GFD) on CD-related neurological manifestations. Early recognition of neurological signs and their prompt management are essential to mitigate irreversible neural injury and improve long-term outcomes in these patients. Given the potential for symptom reversibility with dietary treatment, routine screening for CD should be considered in patients presenting with idiopathic neurological syndromes, even in the absence of GI symptoms.</p>","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"28 1","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707281","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}