Neurological research and practice最新文献

{"title":"Preventive strategies against brain metastases: current state of the art and future directions.","authors":"Franziska Maria Ippen, Franz Felix Konen, Peter Hau, Frank Winkler","doi":"10.1186/s42466-026-00467-7","DOIUrl":"10.1186/s42466-026-00467-7","url":null,"abstract":"<p><p>BACKGROUND: Brain metastases (BM) represent a deleterious complication in many solid tumors. Despite advances in systemic therapy, BM are still associated with significant morbidity and mortality. Consequently, preventive strategies are gaining importance and represent a dynamic area of investigation. METHODS: Relevant literature and clinical trials were included, focusing on systemic therapies, multimodal treatment approaches, and future therapeutic avenues. Clinical trials reporting on secondary (preventing BM in a yet BM-free cancer patient) and tertiary prevention (preventing formation of new and recurrence of existent BM in a patient who has already developed BM) were included. RESULTS: A number of BM treatment-effective drugs have shown BM-preventive effects: In NSCLC, the EGFR-inhibitor osimertinib and ALK inhibitors like alectinib, brigatinib and lorlatinib lower the incidence of BM. In HER2-positive breast cancer, tucatinib and trastuzumab deruxtecan have preventive activity in patients without BM at baseline. In melanoma, BRAF/MEK inhibition and immunotherapy might be able to delay the onset of BM, although prospective data remains limited to date. Notably, drugs effective in BM therapy do not necessarily work in BM prevention, and vice versa. Preclinical data, including insights from Cancer Neuroscience, reveal novel preventive strategies warranting further exploration. CONCLUSIONS: Preventive strategies against BM in solid tumors are feasible, though data are sparse at this time. Preventing BM requires a personalized, multidisciplinary approach, integrating tumor biology, individual risk assessment, and therapeutic advances. Secondary prevention in patients with BM is as vital as tertiary prevention, warranting prospective validation of preclinical concepts. </p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13045146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147611003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting risk factors and strategies for prevention of peripheral neuropathy: focus on B-vitamin deficiencies and metabolic diseases.","authors":"Petra Baum, Joanna Kosacka, Thomas Ebert","doi":"10.1186/s42466-026-00466-8","DOIUrl":"10.1186/s42466-026-00466-8","url":null,"abstract":"<p><p>BACKGROUND: Polyneuropathy (PN) is a common neurological disorder characterized by sensory, motor, and autonomic dysfunction of peripheral nerves. Its incidence is increasing, especially among the elderly population, making PN a significant and growing public health concern worldwide. MAIN BODY: This review highlights the key risk factors contributing to the development of PN, with a particular focus on nutritional and metabolic etiologies. These include B-vitamin deficiencies, prediabetes, diabetes mellitus, obesity, and treatment-induced neuropathies. The complex interplay of these factors often exacerbates the progression of PN and complicates management. Current preventive approaches and challenges in early detection are also discussed to provide a comprehensive overview of strategies aimed at reducing the disease burden. CONCLUSION: The rising prevalence and disabling nature of PN necessitate urgent public awareness, better screening, and increased healthcare resources. Advancing prevention strategies targeting modifiable risk factors may significantly reduce the impact of PN on patients and healthcare systems alike. </p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13045129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uncovering the metabolic-epigenetic links between gene expression and stroke: insights from lactylation pathway MR study.","authors":"Jiuxu Kan, Yong Hong, Ruoxin Min, Bowen Zhang, Hong Wang","doi":"10.1186/s42466-026-00478-4","DOIUrl":"10.1186/s42466-026-00478-4","url":null,"abstract":"<p><p>BACKGROUND: Lactylation, a novel post-translational modification driven by lactate accumulation, has been implicated in neuroinflammation and metabolic stress. However, its causal relevance to ischemic stroke (IS) and its subtypes—large artery stroke (LAS), cardioembolic stroke (CES), and small vessel stroke (SVS)—remains unknown. METHODS: We conducted a two-sample Mendelian randomization (TSMR) analysis to investigate the causal relationships between lactylation-associated gene expression and IS risk. Lactylation-related genes were identified from a recent literature review and intersected with eQTL data from the eQTLGen Consortium (n = 31,684). Summary statistics for IS and its subtypes were obtained from large-scale GWAS (total cases = 62,100; controls = 1,234,808). Primary analyses used the inverse-variance weighted (IVW) method, complemented by MR-Egger, weighted median, and sensitivity tests to assess heterogeneity and pleiotropy. RESULTS: A total of 15 genes and 274 single nucleotide polymorphisms (SNPs) were included. Elevated expression of SIRT1, SMARCA4, STMN1, and LDHA was significantly associated with increased risk of IS or its subtypes. In contrast, SLC16A1, SIRT3, PFKP, and TKT were inversely associated with stroke risk, suggesting a potential protective role. Most associations were robust across multiple MR models. Pleiotropy and heterogeneity were observed for SMARCA4 in LAS. CONCLUSION: This study provides genetic evidence for the involvement of lactylation-related genes in IS pathogenesis, revealing novel risk-enhancing and protective factors. These findings enhance our understanding of metabolic-epigenetic mechanisms in stroke and suggest potential molecular targets for future interventions. </p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147518012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current perspectives in sudden unexpected death in epilepsy (SUDEP): epidemiology, research approaches and pathways to prevention.","authors":"Catrin Mann, Susanne Schubert-Bast, Felix Rosenow, Adam Strzelczyk","doi":"10.1186/s42466-026-00480-w","DOIUrl":"10.1186/s42466-026-00480-w","url":null,"abstract":"<p><p>People with epilepsy (PWE) are affected not only by the unpredictability of seizures, the risk of accidents, stigma, and comorbidities, but also by increased mortality. The most common directly epilepsy‑associated cause of death is sudden unexpected death in epilepsy patients (SUDEP). Across all PWE, SUDEP affects approximately 1 in 1,000 patients per year; depending on epilepsy severity, the annual SUDEP rate can exceed 10 per 1,000 patient years. Because many PWE live with the disorder for several decades, the cumulative SUDEP risk amounts to an average lifetime risk of 5–20%, rendering SUDEP a relevant contributor to mortality in PWE; however, considering its comparatively low annual incidence, SUDEP research remains challenging. Established risk factors and associated patient characteristics include frequent bilateral tonic–clonic seizures (BTCS) -especially when nocturnal-, living alone, long duration of epilepsy, and drug-resistant epilepsy. There are few observations in humans regarding the pathophysiological mechanisms underlying SUDEP, supplemented by findings from registries, animal models, and theoretical considerations. In the typical SUDEP cascade, a pathologically impaired arousal following a preceding, often nocturnal, BTCS appears to precipitate apnea and consequent bradycardia, progressing to fatal asystole. Various individual vulnerability factors contribute to this cascade. However, many aspects remain poorly understood. Two large, recently published prospective cohort studies have contributed valuable insights into biomarkers of SUDEP. Perisylvian epilepsies were identified as risk factors; furthermore, findings suggest dysfunctional brainstem respiratory regulation and impaired sleep homeostasis as potential mechanisms contributing to SUDEP. Nevertheless, on an individual level, it remains poorly understood why some patients die in the context of their first ever epileptic seizure, while others survive hundreds of BTCS. This narrative review provides an overview of the current state of SUDEP research and information on preventive measures used today, and delineates prospective directions for future investigation and prevention.</p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13014865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping neurogenic dysphagia diagnostics in Germany: accessibility, implementation practices, and barriers to swallowing endoscopy.","authors":"Julia Gelenar Marae, Lars Masanneck, Marc Pawlitzki, Cinja Huber, Jule Hofacker, Sriramya Lapa, Anne Jung, Paul Muhle, Sonja Suntrup-Krueger, Tobias Warnecke, Sven G Meuth, Rainer Dziewas, Bendix Labeit","doi":"10.1186/s42466-026-00473-9","DOIUrl":"10.1186/s42466-026-00473-9","url":null,"abstract":"<p><p>BACKGROUND: Flexible Endoscopic Evaluation of Swallowing (FEES) is a core diagnostic tool in neurogenic dysphagia. Despite a structured national training curriculum in Germany, little is known about current implementation practices and outpatient accessibility. This study mapped nationwide FEES practice patterns, workforce structures, and geographic access, and identified barriers to comprehensive service provision. METHODS: A nationwide web-based survey was conducted among certified FEES instructors in Germany. The survey assessed provider characteristics, implementation practices, diagnostic–therapeutic integration, and perceived systemic barriers. In parallel, institutional websites were screened for publicly advertised outpatient FEES services and geocoded for travel-time isochrone analyses. RESULTS: Eighty-two instructors completed the anonymous survey (response rate 52.6%). FEES was predominantly delivered in acute hospitals (74%) and rehabilitation clinics (46%) and embedded within interdisciplinary workflows. Outpatient availability remained limited (54%), with most institutions lacking statutory reimbursement pathways; additionally, many existing outpatient services were not visible to patients online. Geospatial analysis revealed substantial regional disparities, particularly in rural and eastern regions, with only a minority of residents able to reach a publicly identifiable outpatient FEES provider within 30 min. Procedural experience varied widely, and higher monthly FEES volumes were associated with shorter examination duration (r = − 0.27, p = 0.020). CONCLUSIONS: FEES is well implemented in German inpatient dysphagia care but structurally underdeveloped in the outpatient sector. Insufficient reimbursement, workforce shortages, and lack of transparency significantly impede equitable access. Strengthening outpatient infrastructure, establishing sustainable reimbursement mechanisms, and improving national visibility of services are critical steps toward ensuring continuity of dysphagia care. </p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13001358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147483129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Collaborative neurocardiology board meetings for decision-making in stroke care: a real-world experience.","authors":"V Mafael, T Buck, H Stengl, S Hellwig, M G Klammer, M Endres, M Reinthaler, F Barbieri, H J Audebert, D M Leistner, U Landmesser, W Doehner, C Skurk, J F Scheitz","doi":"10.1186/s42466-026-00472-w","DOIUrl":"10.1186/s42466-026-00472-w","url":null,"abstract":"","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter to the editor, regarding \"Acute care of spontaneous intracerebral haemorrhage\", recently published by Shah and colleagues.","authors":"Matija Zupan, Mišo Šabovič, Pawel Kermer, Senta Frol","doi":"10.1186/s42466-026-00475-7","DOIUrl":"10.1186/s42466-026-00475-7","url":null,"abstract":"","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147476635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wearable sensor measurements in relation to clinical characteristics and mortality in patients with Parkinson's disease.","authors":"Daniel von Below, Susanna M Wallerstedt, Filip Bergquist","doi":"10.1186/s42466-026-00474-8","DOIUrl":"10.1186/s42466-026-00474-8","url":null,"abstract":"<p><p>BACKGROUND: Parkinson’s disease (PD) is highly variable between patients, and regular assessments are needed to adjust symptomatic treatment. Wearable sensor measurements can complement clinical examinations and patient-reported outcome measures in the management of PD, but their clinical usefulness is yet to be established. Previous studies have described wearable sensor measurements from selected patients, often with advanced disease, but not PD patients in general. We sought to objectively describe daily-life movement characteristics of population-representative patients with PD using the wrist-worn Personal KinetiGraph (PKG), and to relate these sensor measurements to clinical data and proposed PKG-based treatment targets. METHODS: Individuals in a population-based random sample of patients with PD were evaluated with clinical assessments, patient-reported outcome measures and six-day PKG recordings. PKG outcomes included bradykinesia score (BKS) and dyskinesia score (DKS), reflecting symptom severity. Mortality within eight years was recorded. RESULTS: The study included 286 patients with a median age of 73 years and a median time since diagnosis of five years. Clinical and patient-reported variables expected to increase with disease or symptom severity were positively correlated with bradykinesia score (BKS) and negatively correlated with dyskinesia score (DKS). Patients with BKS > 25 had lower levodopa-equivalent daily dose, higher self-reported symptom burden and lower health-related quality of life compared to patients with BKS ≤ 25. Age- and sex-adjusted mortality rates were 1.8 times higher in patients with BKS > 25. CONCLUSIONS: Sensor-based motor assessments with PKG reflect clinical outcome measures in population-representative PD patients. A high degree of sensor-assessed bradykinesia (BKS > 25) at baseline was associated with higher mortality, shorter disease duration and less intensive treatment. The results suggest that high BKS is a risk factor for mortality, possibly as a marker of undertreatment. TRIAL REGISTRATION: ClinicalTrials.gov identifier NCT03130595, registration date 22 April 2017. </p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147438557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intracranial hemorrhage after ischemic stroke in patients on direct oral anticoagulants: results from a prospective observational study.","authors":"Jan C Purrucker, Kirsten Haas, Marilen Sieber, Viktoria Rücker, Uwe Malzahn, Karl Georg Haeusler, Christian H Nolte, Maria Magdalena Gabriel, Johannes Schiefer, Sven Poli, Dominik Michalski, Hassan Soda, Georg Royl, Johannes Meyne, Darius G Nabavi, Pascal Mosimann, Adrian Heeger, David Kinzler, Patrick Müller, Pascal Rappard, Timolaos Rizos, Peter U Heuschmann, Roland Veltkamp","doi":"10.1186/s42466-026-00462-y","DOIUrl":"10.1186/s42466-026-00462-y","url":null,"abstract":"<p><p>BACKGROUND: Approximately 10% of ischemic strokes occur in patients on oral anticoagulants (OAC), yet prospective data on hemorrhagic complications after recanalization therapies remain limited. We aimed to assess whether prior use of OAC increases the risk of intracranial hemorrhage compared to no anticoagulation in clinical routine. METHODS: The prospective, multicenter RASUNOA-Prime study (clinicaltrials.gov, NCT02533960) enrolled patients with atrial fibrillation and acute ischemic stroke who were receiving a direct OAC (DOAC), a vitamin K antagonist (VKA), or no anticoagulant (non-OAC) at stroke onset. The primary endpoint was symptomatic intracranial hemorrhage (sICH) on follow-up imaging (≤ 120 h after admission), adjusted for thrombolytic therapy. Neuroimaging was centrally reviewed, blinded to treatment group. RESULTS: Among 2,737 patients (median age 79 years, 49% female) from 46 stroke centers (DOAC n = 1,066; VKA n = 695; non-OAC n = 976), stroke severity was lower in DOAC thanin non-OAC patients (median NIHSS 4 [interquartile range (IQR) 2–9] vs. 6 [3–13]). Among those presenting within 4.5 h, thrombolysis was used less often in DOAC than in non-OAC patients (10.0% vs. 58.9%, p < 0.001), with longer door-to-needle time (+ 19 min). The proportion of patients with any hemorrhagic transformation on admission was similar between groups. Follow-up imaging and clinical data on sICH were available for 1,813 patients (66%). Symptomatic ICH occurred in 0.59% (95% CI 0.01–1.17) of DOAC, 1.09% (95% CI 0.14–2.03) of VKA and 1.18% (95% CI 0.37–1.99) of non-OAC patients. After adjusting for thrombolysis, the odds of sICH were comparable across anticoagulation groups (adjusted OR 1.46, 95% CI 0.36–5.92, p = 0.6 for DOAC; adj. OR 1.43, 95% CI 0.43–4.70, p = 0.56 for VKA). CONCLUSIONS: The risk of sICH was not increased with DOAC use compared to no anticoagulation after ischemic stroke, with or without thrombolysis. Although event rates were low and confidence intervals wide, the findings suggest non-inferiority but cannot exclude a modest increase in bleeding risk. Randomized trials are warranted to confirm safety in this population. </p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12947503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147313838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of predictors indicating paroxysmal atrial fibrillation in patients with acute ischemic strokes: the Find-AF_RANDOMISED trial.","authors":"Mark Weber-Krüger, Antonia Zapf, Evgeny Protsenko, Jan Liman, Gerhard F Hamann, Pawel Kermer, Katrin Wasser, Timo Uphaus, Sonja Gröschel, Klaus Gröschel, Rolf Wachter","doi":"10.1186/s42466-026-00471-x","DOIUrl":"10.1186/s42466-026-00471-x","url":null,"abstract":"<p><p>BACKGROUND: Detecting concealed paroxysmal atrial fibrillation after stroke requires elaborate electrocardiographic monitoring. We evaluated previously established predictors to quantify the individual risk of detecting atrial fibrillation within six months in the Find-AFRANDOMISED-trial. METHODS: We analyzed 200 patients ≥ 60 years with acute ischemic strokes in the intervention arm of the Find-AFRANDOMISED-trial. Patients received three ten-day Holter-electrocardiograms within six months. Regression analyses and receiver-operator-characteristics were used to select promising biomarkers and assess predictive performance. We applied previously established cut-offs for the most promising markers to determine those at a high risk of underlying atrial fibrillation. RESULTS: 27/200 patients (13.5%) had atrial fibrillation after six months. The left atrial diameter, atrial premature beats, supraventricular runs and brain natriuretic peptide were associated with atrial fibrillation, whereas the established markers age and suspected stroke etiology were not. Atrial premature beats differentiated best between those with and without atrial fibrillation (area-under-the-curve = 0.75). Only brain natriuretic peptide ≥ 100pg/ml and supraventricular runs ≥ 20 beats independently predicted atrial fibrillation in multivariable models. CONCLUSIONS: Supraventricular runs and brain natriuretic peptide were the most promising predictors to define a high risk of underlying atrial fibrillation after stroke in our study. Future screening strategies for atrial fibrillation in stroke patients should focus on these parameters rather than the suspected stroke etiology. TRIAL REGISTRATION: clinicaltrials.gov NCT01855035 registered 05132013 https//www.clinicaltrials.gov/study/NCT01855035?tab=table. </p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"8 1","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147278098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}