Journal of neural transmission (Vienna, Austria : 1996)最新文献

{"title":"The enigma of vascular dementia: current state and emerging perspectives.","authors":"Kurt A Jellinger","doi":"10.1007/s00702-026-03104-4","DOIUrl":"10.1007/s00702-026-03104-4","url":null,"abstract":"","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"1979-2021"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146014153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CSF protein biomarkers are associated with atrophy and symptom severity in genetic FTD: a GENFI study.","authors":"Abbe Ullgren, Melissa Taheri Rydell, Sofia Bergström, Linn Öijerstedt, Jennie Olofsson, Arabella Bouzigues, Lucy L Russell, Phoebe H Foster, Eve Ferry-Bolder, John C van Swieten, Lize C Jiskoot, Harro Seelaar, Raquel Sanchez-Valle, Robert Laforce, Daniela Galimberti, Rik Vandenberghe, Alexander Gerhard, Simon Ducharme, Christopher R Butler, Elizabeth Finger, Maria Carmela Tartaglia, Mario Masellis, James B Rowe, Matthis Synofzik, Fermin Moreno, Barbara Borroni, Jonathan D Rohrer, Peter Nilsson, Elena Rodriguez-Vieitez, Anna Månberg, Eric Westman, Caroline Graff","doi":"10.1007/s00702-026-03118-y","DOIUrl":"10.1007/s00702-026-03118-y","url":null,"abstract":"<p><p>Over the past few years, several fluid biomarker candidates have been proposed for frontotemporal dementia (FTD). We have previously identified CSF proteins that could separate individuals with genetic FTD from controls. However, it is unknown whether alterations in these CSF protein levels are associated with neurodegenerative processes. The aim of this study was to explore how these CSF biomarker candidates correlate with symptom severity as well as cortical and subcortical atrophy. The levels of fourteen proteins were measured in CSF from 202 individuals, 131 mutation carriers with mutations in C9orf72, GRN, or MAPT, and 71 controls, in a cross-sectional subset from the GENFI cohort. The association between the levels of these proteins and CDR plus NACC FTLD-NM sum-of-boxes, cortical thickness, and subcortical volumes were estimated in the mutation carriers. Elevated CSF levels of five out of fourteen proteins were associated with an increased CDR score in the mutation carriers. Additionally, elevated levels of three of these proteins, NEFM, PTPRN2 and SERPINA3, were associated with reduced cortical thickness and/or subcortical volume among all mutation carriers. Some mutation-specific associations were also observed, with SPP1 and CTSS being associated with CDR and atrophy only in MAPT mutation carriers, while NPTX2 was specific for GRN mutation carriers. As indicated by the association to brain atrophy, the proposed fluid biomarker candidates continue to show promise and additional studies will further elucidate their relationship to cortical atrophy in genetic FTD, and their potential as biomarkers for diagnosis, prognosis, and disease staging.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2339-2347"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146230412","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":"Association between BDNF methylation and expression of the NLRP3 inflammasome in the brain is disrupted in Alzheimer's disease.","authors":"Hao Tang, Helene A Fachim, Michael K Harte, Gavin P Reynolds","doi":"10.1007/s00702-026-03280-3","DOIUrl":"10.1007/s00702-026-03280-3","url":null,"abstract":"<p><p>Activation of the NLRP3 inflammasome pathway and dysfunction of brain-derived neurotrophic factor (BDNF) are both implicated in the pathogenesis of Alzheimer's disease (AD). While in vitro and in vivo models support these mechanisms, there is little research investigating their relationship in human brain tissue, and whether this relationship may be abnormal in the AD brain. Temporal cortex tissue taken post-mortem from AD patients and control subjects was analysed for expression of genes for the NLRP3 pathway (NLRP3, PYCARD, CASP1), the potassium channel THIK1 (KCNK13), and related pro-inflammatory cytokines (IL-1β, IL-18). BDNF mRNA expression and DNA methylation in the BDNF exon IV promoter were determined. Correlations between these BDNF measures and NLRP3-related genes were investigated. A significant relationship between BDNF mRNA expression and mean methylation was observed in control subjects but not in AD. In controls, significant correlations with both BDNF expression and mean BDNF methylation were observed for NLRP3, CASP1 and IL1B. These correlations were lost in the AD group, which also showed a significant correlation of KCNK13 expression with both BDNF measures, not seen in controls. This study indicates that the relationship between BDNF and NLRP3 activation, as measured by NLRP3 inflammasome components and proinflammatory cytokine products, is disrupted in AD. The contrary correlation emerging in AD between BDNF measures and KCNK13 expression, shown to be elevated in AD, indicates the possible relationship of this finding with BDNF dysfunction. These findings enhance our understanding of AD pathophysiology, demonstrating the importance of understanding the neuroinflammatory-neurotrophic balance in neurodegenerative processes.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2831-2837"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149122789","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":"Functional brain imaging in posttraumatic stress disorder: a review.","authors":"J Douglas Bremner","doi":"10.1007/s00702-026-03228-7","DOIUrl":"10.1007/s00702-026-03228-7","url":null,"abstract":"<p><p>Posttraumatic stress disorder (PTSD) is associated with symptoms of intrusive memories, avoidance, and hyperarousal. Accumulated evidence shows that these symptoms are related to changes in brain areas involved in memory and emotion. The purpose of this paper was to review functional brain imaging studies in PTSD. Pubmed, midline, and psych info were queried for keywords related to PTSD and brain imaging from 1990-2024. The review focused on functional brain imaging using Positron Emission Tomography (PET), single photon emission tomography (SPECT) and functional magnetic resonance imaging (fMRI) and did not include structural or spectroscopic imaging. Studies implicated a network of brain regions involved in memory and emotion including the amygdala, insula, prefrontal cortex, cingulate gyrus and hippocampus. PTSD is associated with alterations in function in brain areas mediating memory and emotion.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2247-2266"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148805142","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":"Pain characteristics in isolated cervical dystonia: comparison to orthopedic cervical conditions and assessment of botulinum toxin effects.","authors":"L Vorbeck, L Herrmann, A Palisi, S Lezius, A Maurer, M Dreimann, M Gelderblom, J Mallwitz, Simone Zittel","doi":"10.1007/s00702-026-03276-z","DOIUrl":"10.1007/s00702-026-03276-z","url":null,"abstract":"<p><p>The objective was to characterize pain and evaluate quality of life (QoL) in cervical dystonia (CD) by comparing pain profiles with patients affected by orthopedic cervical conditions (OCC) and evaluating differences between CD patients with and without head tremor (HT). Additionally, longitudinal changes after botulinum toxin (BoNT) treatment in CD were assessed. Pain is the most prevalent non-motor symptom in CD. However, its clinical characteristics and underlying mechanisms are incompletely understood. Isolated CD and OCC patients were evaluated regarding pain characteristics and QoL using self-report questionnaires. CD patients additionally underwent blinded motor assessment and were stratified according to the presence of HT. A subset of CD patients was reevaluated 4-6 weeks after BoNT treatment. 49 CD patients and 49 OCC patients were investigated. The overall pain profile was comparable between CD and OCC; only nociceptive pain perception was higher in OCC than in CD. HT in CD patients was associated with increased nociceptive pain and greater QoL impairment. Following BoNT injection in CD, pain and QoL improved significantly. The marked similarities of pain profiles in CD and OCC together with the increased nociceptive pain in CD patients with HT suggest that musculoskeletal mechanisms contribute to pain in CD. Improvement of pain and QoL in CD patients with long disease duration after BoNT treatment indicates the relevant effect on non-motor symptoms. Further studies are needed to clarify the underlying pathophysiology of pain in CD.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2799-2807"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149043276","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":"Screening speech disorders in progressive neurological diseases via long-term average spectrum.","authors":"Jan Svihlik, Jan Rusz","doi":"10.1007/s00702-026-03176-2","DOIUrl":"10.1007/s00702-026-03176-2","url":null,"abstract":"<p><p>The long-term averaged spectrum (LTAS) may provide a universal method for capturing distinct patterns of dysarthria. This study aimed to evaluate the sensitivity of LTAS descriptors in a broad range of neurological diseases and various types and severities of dysarthria. Four spectral moments of spectral mean, spectral standard deviation, spectral skewness and spectral kurtosis based on LTAS were computed for reading passage collected from 461 speakers, including 306 healthy controls and 155 neurological patients secondary to Parkinson's disease (PD), progressive supranuclear palsy, multiple system atrophy (MSA), Huntington's disease, essential tremor, cerebellar ataxia (CA), multiple sclerosis (MS), and amyotrophic lateral sclerosis. Compared to controls, the spectral mean was significantly lower in PD and MS while elevated in CA. Significantly changed LTAS features were observed only in hypokinetic dysarthria and in mixed dysarthrias manifesting hypokinetic elements. Although LTAS features differed between controls and patients with varying degrees of dysarthria, there was no progressive increase in dysarthria severity. Our findings suggest that LTAS-based speech analysis may provide valuable cues to aid differential diagnosis among neurological diseases with overlapping clinical features. LTAS appears more informative when applied to specific diseases than to pooled dysarthria types arising from diverse neurological etiologies.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2493-2502"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147944592","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":"Long-term efficiency of pallidal DBS and the role of Levodopa treatment in DYT-GNAL and 18p deletion syndrome associated dystonia: an observational study and review of literature.","authors":"Johanna Reimer, Friederike Schumann, Katja Lohmann, Thomas G Riemer, Joachim K Krauss, Gerd-Helge Schneider, Andrea A Kühn, Patricia Krause","doi":"10.1007/s00702-026-03109-z","DOIUrl":"10.1007/s00702-026-03109-z","url":null,"abstract":"<p><p>Dystonia due to loss-of-function variants in the GNAL gene in DYT-GNAL and 18p-deletion (18pdel) syndrome has been reported to respond well to pallidal deep brain stimulation (GPi-DBS) occasionally, but long-term data is scarce. GNAL is implicated in dopamine receptor function, which may explain anecdotal reports of hypokinesia in DYT-GNAL and 18pdel-associated dystonia, a phenomenon that has not yet been systematically reviewed. We retrospectively evaluated a cohort of three patients with GNAL variants treated with GPi-DBS, documenting individual long-term outcomes spanning up to 25 years. Dystonia severity was assessed using the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) and the Burke - Fahn - Marsden Dystonia Rating Scale (BFMDRS). We also documented bradykinetic symptoms and levodopa response. A literature review was added focusing on DBS outcomes and the effects of levodopa in DYT-GNAL and 18pdel-associated dystonia. In our patients, TWSTRS severity subscale I was reduced by 63% in early (≤ 12months; 20.7 to 7.7 points) and 81% in late follow-up (> 12months; 20.7 to 4 points) after GPi-DBS χ. BFMDRS decreased by 67% and 44%; each with a Kendall's coefficient of 0.78, indicating a high degree of concordance in improvement trajectories. Two patients exhibited bradykinesia, which was levodopa-responsive in one. GPi-DBS responses have been reported for another ten DYT-GNAL and two 18pdel-patients. Bradykinesia prompted levodopa challenges in 15 patients, resulting in improvement in five. Long-term follow-up data from three DYT-GNAL patients treated with DBS showed sustained improvement in dystonia, particularly in cervical symptoms. Bradykinesia may be an inherent clinical feature of GNAL-related dystonia, warranting further investigation.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2907-2916"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146115152","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":"History of childhood trauma enhances the detrimental effects of recent stressors on brain structure and function in major depressive disorder.","authors":"Serena Furno, Marco Paolini, Chiara Milano, Virginia Saredi, Laura Raffaelli, Raffaella Zanardi, Cristina Colombo, Francesco Benedetti, Sara Poletti","doi":"10.1007/s00702-026-03273-2","DOIUrl":"10.1007/s00702-026-03273-2","url":null,"abstract":"<p><p>Stressful life events are major precipitants of depressive episodes, yet their effects vary across individuals. Childhood trauma is a well-established vulnerability factor that may increase sensitivity to subsequent stress. However, the neural correlates of this interaction in major depressive disorder (MDD) remain poorly characterized. This study investigated whether childhood trauma moderates the association between recent stress exposure and brain structure and functional connectivity in MDD. Structural magnetic resonance imaging (MRI) data were obtained from 130 inpatients with MDD; resting-state functional MRI data were available for a subsample (n = 97). Whole-brain cortical thickness and surface-based functional connectivity measures, including global correlation (GCOR) and local correlation (LCOR), were examined to test interaction effects between childhood trauma and recent stress exposure. A significant interaction between childhood trauma and recent stress was observed in medial prefrontal regions, including the anterior cingulate cortex, where greater stress exposure was associated with reduced cortical thickness at higher levels of early adversity. Convergent interaction effects were also observed at the functional level, with greater recent stress associated with lower LCOR in the left superior frontal gyrus and precuneus at higher levels of childhood trauma. No interaction effects were observed for GCOR. Analyses of specific trauma dimensions indicated partially distinct effects of abuse and neglect. Childhood trauma moderated the association between recent stress exposure and structural and functional brain measures in MDD, particularly within prefrontal regulatory regions. These multimodal findings are consistent with stress sensitization models and suggest that early adversity may contribute to heterogeneity in neural correlates of stress in depression.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2267-2278"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148858068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Childhood maltreatment and inflammatory biomarkers associated with depressive severity in adolescents with major depressive disorder.","authors":"Peiying Li, Wuyou Bao, Shiying Wang, Jiang Wang, Ling Sun, Bin Zhang","doi":"10.1007/s00702-026-03279-w","DOIUrl":"10.1007/s00702-026-03279-w","url":null,"abstract":"<p><p>Adolescent depression shows marked heterogeneity in symptom severity, yet mechanisms linking early-life adversity to severe depressive presentations remain unclear. Childhood maltreatment may induce persistent alterations in immune and stress-regulatory systems, increasing vulnerability to severe depression. This study examined whether childhood adversity, circulating biomarkers, and recent stress contribute to differences between severe and non-severe adolescent depression. Seventy adolescents with depressive disorder were classified into severe (SD, n = 40, HAMD-17 ≥ 24) and non-severe (NSD, n = 30, HAMD-17 < 24) groups, along with 39 healthy controls (HC). Childhood maltreatment was assessed using the Maltreatment and Abuse Chronology of Exposure (MACE), and recent stress using the Adolescent Life Events Scale. Serum levels of Pentraxin-3 (PTX3), S100B, matrix metalloproteinases (MMP-8, MMP-9), FKBP5, oxytocin, epidermal growth factor, and APCDD1 were measured by enzyme-linked immunosorbent assays. Adolescents with SD reported significantly higher childhood maltreatment than those with NSD. PTX3 and FKBP5 levels were significantly elevated in the severe group compared with both non-severe patients and HC and were positively associated with symptom severity. Receiver operating characteristic analyses showed that childhood maltreatment had good discriminative ability for depressive severity, whereas PTX3 and FKBP5 showed moderate discriminative performance. Multivariable logistic regression identified childhood maltreatment and PTX3 as independent predictors of SD. Hierarchical regression showed that recent life stress explained additional variance in self-reported symptom severity and partly attenuated the associations of early adversity and inflammatory markers. These findings suggest that severe adolescent depression represents a clinically defined severity stratum associated with neuroimmune alterations in the context of childhood adversity and recent life stress, rather than a discrete biological subtype.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2819-2830"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148914910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of serotonin transporter deficiency on parvalbumin- and neuropeptide Y-producing neurons of the lateral and basolateral amygdalar nuclei.","authors":"Henning Schwert, Elif Salur, Mirjam Richard, Mara Pöllmann, Klaus-Peter Lesch, Esther Asan, Angelika Schmitt-Böhrer","doi":"10.1007/s00702-026-03224-x","DOIUrl":"10.1007/s00702-026-03224-x","url":null,"abstract":"<p><p>Hyperexcitability of lateral (La) and basolateral (BL) amygdalar nuclei (BLA) is a hallmark of anxiety-related disorders in humans. Excitation of BLA projection neurons (PN) is fine-tuned by inhibitory interneurons (INs), and monoaminergic afferents to the BLA modulate PN and IN activity. In the present study, BLA-neurons immunoreactive(ir) for parvalbumin (PV) or neuropeptide Y (NPY) and their interrelations with serotonergic and catecholaminergic afferents were analyzed in wildtype (WT) and in serotonin (5-HT) transporter knockout (5-HTT KO) mice, a mouse model for anxiety- and stress-related disorders. In both genotypes, PV- and NPY-ir neurons possess perisomatic appositions by serotonergic and tyrosine hydroxylase-ir afferents. Dual immunolabeling shows no colocalization of PV and NPY. Qualitative analysis of NPY/somatostatin(SOM) dual labeling in WT and 5-HTT KO mice documents colocalization of the peptides in neurons with predominantly fusiform somata, and single labeling for NPY in neurons with predominantly round somata. Quantification of PV- and NPY-ir neurons documents a reduction in numbers and densities of NPY-ir neurons of the BLA in 5-HTT KO mice while PV-ir neuron numbers and densities remain unchanged. Quantitative PCR shows increased expression of Npy receptor 2, Som receptor 4, and corticotropin releasing factor receptor 1 in the BLA of 5-HTT KO mice. mRNA for the peptides is unchanged, indicating that it may be NPY propeptide translation which is reduced in 5-HTT KO mice. Taken together, the results document an effect of life-long serotonin imbalance on the BLA NPY-system, which may contribute to increased anxiety-like behavior in 5-HTT KO mice.</p>","PeriodicalId":520679,"journal":{"name":"Journal of neural transmission (Vienna, Austria : 1996)","volume":" ","pages":"2635-2660"},"PeriodicalIF":4.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148805140","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}