Brain最新文献

{"title":"Hypometabolic mismatch with atrophy and tau pathology in mixed Alzheimer's and Lewy body disease.","authors":"Michael Tran Duong, Sandhitsu R Das, Pulkit Khandelwal, Xueying Lyu, Long Xie, Emily McGrew, Nadia Dehghani, Corey T McMillan, Edward B Lee, Leslie M Shaw, Paul A Yushkevich, David A Wolk, Ilya M Nasrallah","doi":"10.1093/brain/awae352","DOIUrl":"10.1093/brain/awae352","url":null,"abstract":"<p><p>Polypathology is a major driver of heterogeneity in the clinical presentation and extent of neurodegeneration (N) in patients with Alzheimer's disease (AD). Beyond amyloid (A) and tau (T) pathologies, over half of patients with AD have concomitant pathology such as α-synuclein (S) in mixed AD with Lewy body disease (LBD). Patients with multiple aetiology dementia such as AD + LBD have faster progression and potentially differential responses to targeted treatments, although the diagnosis of AD + LBD can be challenging given the overlapping clinical and imaging features. Development and validation of improved in vivo biomarkers are required to study relationships between N and S and identify imaging patterns reflecting mixed AD + LBD pathologies. We hypothesized that individual proteinopathies, such as T and S, are associated with commensurate levels of N. Thus, we assessed biomarkers of A, T, N and S with PET, MRI and CSF seeding amplification assay (SAA) data to determine molecular presentations of mixed A+S+ versus A+S- cognitively impaired patients from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Strikingly, A+S+ patients had parieto-occipital 18F-fluorodeoxyglucose hypometabolism (a measure of N) disproportionate to the degree of regional atrophy or T burden, highlighting worse hypometabolism associated with S+ status on SAA. Following up on this hypometabolic mismatch with CSF metabolite and proteome analyses, we found that A+S+ patients exhibited lower CSF levels of dopamine metabolites and synaptic markers like neuronal pentraxin-2 (NPTX2), suggesting that altered neurotransmission and neuron integrity contribute to this dissociation between metabolic PET and MRI. Potential confounders exist when studying relations between N, AD and LBD pathologies, including neuroinflammation and other non-Alzheimer's pathologies in mixed dementia, although our findings imply posterior hypometabolic mismatch is related more to S than vascular or TDP-43 pathology. Overall, A+S+ patients had posterior mismatch with excessive 18F-fluorodeoxyglucose hypometabolism relative to atrophy or T load, possibly reflecting impaired neuronal integrity. Further research must disentangle the impact of multiple proteinopathies and clinicopathologic factors on hypometabolism and atrophy. Cumulatively, patients with mixed AD + LBD aetiologies harbour a unique metabolic PET mismatch signature.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"1577-1587"},"PeriodicalIF":10.6,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12073973/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142685913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding brain calcification via N-terminal acetylation at the Golgi apparatus","authors":"Anette Siggervåg, Åse K Bekkelund, Jaakko Saraste, Henriette Aksnes","doi":"10.1093/brain/awaf175","DOIUrl":"https://doi.org/10.1093/brain/awaf175","url":null,"abstract":"Primary familial brain calcification (PFBC) provides valuable insights into the mechanisms underlying brain calcification as it singles out the proteins that potentially are involved in the relevant cellular pathways. To date, seven genes have been linked to PFBC, and studying their encoded proteins marks an exciting new era in understanding the disease mechanisms, which may ultimately lead to therapeutic strategies to prevent brain calcification. With each new gene found to be associated with PFBC due to pathogenic variants, an additional level of understanding is achieved. Here, we highlight the most recently discovered PFBC gene, encoding the Golgi-localized N-terminal acetyltransferase NAA60. We explore the novel perspectives gained from the understanding of this enzyme’s molecular, cellular and physiological properties. Interestingly, NAA60 shares a critical role with the most frequent PFBC gene, SLC20A2. Both these proteins seem to be involved in maintaining the structural integrity of the Golgi apparatus, as deficiency in either protein leads to Golgi fragmentation. Altered Golgi morphology is therefore emerging as a new significant topic in PFBC research, and we here discuss this topic in relation to existing knowledge regarding Golgi rearrangements and dysfunction as a factor in neurodegenerative diseases.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"140 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143930864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional contribution of astrocytic Kir4.1 channels to spasticity after spinal cord injury","authors":"Tony Barbay, Emilie Pecchi, Jorge Ramirez-Franco, Anton Ivanov, Frédéric Brocard, Nathalie Rouach, Rémi Bos","doi":"10.1093/brain/awaf147","DOIUrl":"https://doi.org/10.1093/brain/awaf147","url":null,"abstract":"Spasticity, a prevalent motor issue characterized by network hyperexcitability, causes pain and discomfort, with existing treatments offering limited relief. While past research has focused on neuronal factors, the role of astrocytes in spasticity has been overlooked. This study explores the potential of restoring astrocytic potassium (K+) uptake to reduce spasticity following spinal cord injury (SCI). Astrocytes buffer extracellular K+ via Kir4.1 channels, preventing neuronal hyperexcitability. Following SCI, Kir4.1 levels decrease at the injury site, though the consequences and mechanisms of this reduction within the motor output area have not been investigated. We here demonstrate that lumbar astrocytes in a juvenile thoracic SCI mouse model switch to a reactive phenotype, displaying morpho-functional and pro-inflammatory changes. These astrocytes also experience NBCe1-mediated intracellular acidosis, leading to Kir4.1 dysfunction and impaired K+ uptake. Enhancing Kir4.1 function reduces spasticity in SCI mice, revealing new therapeutic targets for neurological diseases associated with neuronal hyperexcitability.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"16 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnosing migraine from genome-wide genotype data: a machine learning analysis.","authors":"Antonios Danelakis,Tjaša Kumelj,Bendik S Winsvold,Marte Helene Bjørk,Parashkev Nachev,Manjit Matharu,Dominic Giles,,Erling Tronvik,Helge Langseth,Anker Stubberud","doi":"10.1093/brain/awaf172","DOIUrl":"https://doi.org/10.1093/brain/awaf172","url":null,"abstract":"Migraine has an assumed polygenic basis, but the genetic risk variants identified in genome-wide association studies only explain a proportion of the heritability. We aimed to develop machine learning models, capturing non-additive and interactive effects, to address the missing heritability. This was a cross-sectional population-based study of participants in the second and third Trøndelag Health Study. Individuals underwent genome-wide genotyping and were phenotyped based on validated modified criteria of the International Classification of Headache Disorders. Four datasets of increasing number of genetic variants were created using different thresholds of linkage disequilibrium and univariate genome-wide associated p-values. A series of machine learning and deep learning methods were optimized and evaluated. The genotype tools PLINK and LDPred2 were used for polygenic risk scoring. Models were trained on a partition of the dataset and tested in a hold-out set. The area under the receiver operating characteristics curve was used as the primary scoring metric. Classification by machine learning was statistically compared to that of polygenic risk scoring. Finally, we explored the biological functions of the variants unique to the machine learning approach. 43,197 individuals (51% women), with a mean age of 54.6 years, were included in the modelling. A light gradient boosting machine performed best for the three smallest datasets (108, 7,771 and 7,840 variants), all with hold-out test set area under curve at 0.63. A multinomial naïve Bayes model performed best in the largest dataset (140,467 variants) with a hold-out test set area under curve of 0.62. The models were statistically significantly superior to polygenic risk scoring (area under curve 0.52 to 0.59) for all the datasets (p<0.001 to p=0.02). Machine learning identified many of the same genes and pathways identified in genome-wide association studies, but also several unique pathways, mainly related to signal transduction and neurological function. Interestingly, pathways related to botulinum toxins, and pathways related to the calcitonin gene-related peptide receptor also emerged. This study suggests that migraine may follow a non-additive and interactive genetic causal structure, potentially best captured by complex machine learning models. Such structure may be concealed where the data dimensionality (high number of genetic variants) is insufficiently supported by the scale of available data, leaving a misleading impression of purely additive effects. Future machine learning models using substantially larger sample sizes could harness both the additive and the interactive effects, enhancing precision and offering deeper understanding of genetic interactions underlying migraine.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"26 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondria as the key to understanding neuroinflammation.","authors":"Tamas Kozicz,Eva Morava","doi":"10.1093/brain/awaf173","DOIUrl":"https://doi.org/10.1093/brain/awaf173","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":"43 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The case for targeting latent and lytic Epstein-Barr virus infection in multiple sclerosis.","authors":"Gavin Giovannoni,Louisa James,Adekunle A Adeniran,Julian Gold,Lawrence S Young,David L Selwood,David Baker,Ruth Dobson","doi":"10.1093/brain/awaf170","DOIUrl":"https://doi.org/10.1093/brain/awaf170","url":null,"abstract":"Epstein-Barr virus (EBV) is strongly associated with multiple sclerosis (MS). It is likely to play a causal role in the pathogenesis of MS, possibly via triggering autoimmunity through molecular mimicry, autoantigenic presentation or immune dysregulation. Alternatively, evidence supports a direct role for EBV in driving MS disease activity via latent-lytic infection cycling either within the central nervous system or the periphery. We highlight the recent immunological and virological findings supporting the role of active EBV infection in MS, supporting an evaluation of anti-EBV strategies as potential treatments for MS. Anti-EBV strategies include CNS penetrant small molecule anti-viral agents targeting latent and lytic infection, and immunotherapies. Immunotherapies include EBV-specific autologous or allogeneic cytotoxic T-cells (CTL) and therapeutic EBV vaccines and/or immune checkpoint inhibitors to rejuvenate and boost endogenous EBV-targeted CTL responses. In parallel, several licensed MS disease-modifying therapies may work via mechanisms targeting EBV directly or indirectly. B-cell depleting therapies have been shown to have anti-EBV activity; additionally new strategies to target intrathecal B-cells, plasmablasts and plasma cells are being explored including high-dose anti-CD20 therapy, cladribine, proteasome inhibitors, BTK inhibitors, CNS-penetrant anti-CD20/CD19 monoclonal antibodies and CD19-targeted CAR T-cells. Innovative trial designs for proof-of-concept studies to test EBV antivirals and immunotherapies in MS are needed to catalyse a wave of drug development targeting EBV as a therapeutic strategy to prevent or treat MS.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"67 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"More is more: combining therapies to enhance spinal cord injury recovery","authors":"Paulina S Scheuren, Emmanuel Ogalo, Michael J Berger, John L K Kramer","doi":"10.1093/brain/awaf164","DOIUrl":"https://doi.org/10.1093/brain/awaf164","url":null,"abstract":"This scientific commentary refers to ‘Combinatorial approaches increasing neuronal activity accelerate recovery after spinal cord injury’ by Chen et al. (https://doi.org/10.1093/brain/awaf099).","PeriodicalId":9063,"journal":{"name":"Brain","volume":"24 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143910280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholinergic degeneration in prodromal and early Parkinson's: a link to present and future disease states.","authors":"Tamir Eisenstein,Karolien Groenewald,Ludo van Hillegondsberg,Falah Al Hajraf,Tanja Zerenner,Michael A Lawton,Yoav Ben-Shlomo,Ludovica Griffanti,Michele T Hu,Johannes C Klein","doi":"10.1093/brain/awaf168","DOIUrl":"https://doi.org/10.1093/brain/awaf168","url":null,"abstract":"The neuropathological process in Parkinson's disease (PD) and Lewy body disorders has been shown to extend well beyond the degeneration of the dopaminergic system, affecting other neuromodulatory systems in the brain which play crucial roles in the clinical expression and progression of these disorders. Here, we investigate the role of the macrostructural integrity of the nucleus basalis of Meynert (NbM), the main source of cholinergic input to the cerebral cortex, in cognitive function, clinical manifestation, and disease progression in non-demented subjects with PD and individuals with isolated REM sleep behaviour disorder (iRBD). Using structural MRI data from 393 early PD patients, 128 iRBD patients, and 186 controls from two longitudinal cohorts, we found significantly lower NbM grey matter volume in both PD (β=-12.56, p=0.003) and iRBD (β=-16.41, p=0.004) compared to controls. In PD, higher NbM volume was associated with better higher-order cognitive function (β=0.10, p=0.045), decreased non-motor (β=-0.66, p=0.026) and motor (β=-1.44, p=0.023) symptom burden, and lower risk of future conversion to dementia (Hazard ratio (HR)<0.400, p<0.004). Higher NbM volume in iRBD was associated with decreased future risk of phenoconversion to PD or dementia with Lewy bodies (DLB) (HR<0.490, p<0.016). However, despite similar NbM volume deficits to those seen in PD, associations between NbM structural deficits and current disease burden or clinical state were less pronounced in iRBD. These findings identify NbM volume as a potential biomarker with dual utility: predicting cognitive decline and disease progression in early PD, while also serving as an early indicator of phenoconversion risk in prodromal disease. The presence of structural deficits before clear clinical correlates in iRBD suggests complex compensatory mechanisms may initially mask cholinergic dysfunction, with subsequent failure of these mechanisms potentially contributing to clinical conversion.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"38 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxygen extraction fraction in small vessel disease: relationship to disease burden and progression","authors":"Ruiting Zhang, Miao Lin, Junghun Cho, Xinfeng Yu, Yeerfan Jiaerken, Shuyue Wang, Hui Hong, Xiaojun Guan, Yao Zhang, Linyun Xie, Lingyun Liu, Lei Cui, Minming Zhang, Geert Jan Biessels, Jeroen C W Siero, Peiyu Huang","doi":"10.1093/brain/awae383","DOIUrl":"https://doi.org/10.1093/brain/awae383","url":null,"abstract":"Chronic hypoperfusion has been considered a major mechanism of cerebral small vessel disease. Nonetheless, brain tissue may increase oxygen extraction fraction to mitigate hypoxia and delay parenchymal damage. This study aims to investigate oxygen extraction fraction in cerebral small vessel disease and understand its relationship to disease burden and progression. We retrospectively included 195 patients with cerebral small vessel disease and 178 normal controls. Cerebral blood flow was measured by arterial spin labelling. Oxygen extraction fraction was estimated by quantitative susceptibility mapping plus quantitative blood oxygen-level dependence imaging. We compared baseline cerebral blood flow and oxygen extraction fraction in the whole white matter, normal-appearing white matter and white matter hyperintensities between the patient and control groups. Then, we studied whether cerebral blood flow and oxygen extraction fraction differed among patients with varying disease burdens. Longitudinally, we used linear mixed models to evaluate whether cerebral blood flow and oxygen extraction fraction could together predict the progression of white matter hyperintensities or free water (mean follow-up time = 2.6 years) in a subset of 47 patients. Compared to the control group, the patient group exhibited reduced cerebral blood flow in the whole white matter, normal-appearing white matter and white matter hyperintensities. Additionally, the oxygen extraction fraction increased in normal-appearing white matter but decreased in white matter hyperintensities. Notably, the white matter oxygen extraction fraction was elevated in patients with mild-to-moderate disease burden but decreased in those with the most severe disease burden. Longitudinal analyses revealed that adding oxygen extraction fraction measurements to cerebral blood flow measurements can improve the prediction of disease progression. Higher baseline values of cerebral blood flow and oxygen extraction fraction in the white matter were both linked to a slower increase in free water. In summary, oxygen extraction fraction exhibited an ‘increase-then-decrease’ pattern in patients with cerebral small vessel disease. Together, oxygen extraction fraction and cerebral blood flow can predict disease progression. Non-invasive MRI assessment of oxygen extraction fraction may provide valuable tools for future research on cerebral small vessel disease.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"115 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143910334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Common neuropathologic change drivers of hippocampal sclerosis of ageing","authors":"Davis C Woodworth, Jerry J Lou, William H Yong, Elizabeth Head, María M Corrada, Peter T Nelson, S Ahmad Sajjadi","doi":"10.1093/brain/awaf158","DOIUrl":"https://doi.org/10.1093/brain/awaf158","url":null,"abstract":"Hippocampal sclerosis of aging (HS-A) –severe cell loss and gliosis in the hippocampal formation– is a neuropathologic change (NC) that affects up to 20% of elderly persons with dementia. The etiology of HS-A is heterogeneous, but HS-A is strongly associated with limbic-predominant age-related TDP-43 encephalopathy NC (LATE-NC). Other NCs have also been implicated in relation to HS-A, but these associations have been inconsistent across previous studies. Also, because LATE-NC and HS-A are so strongly associated, it is important to adjust for LATE-NC when examining associations between other NCs and HS-A. The goal of this study was to examine associations of other common NCs with HS-A, both before and after adjusting for LATE-NC. We analyzed the National Alzheimer’s Coordinating Center (NACC) neuropathology dataset and examined associations of Alzheimer’s disease NC (ADNC), Lewy bodies (LB), and cerebrovascular NCs, with HS-A, adjusting for LATE-NC in multiple ways. We used Bayesian multilevel logistic regression models with monotonic modeling for ordinal predictors, and report the odds ratios (OR) or average OR across levels (aOR) along with 95% credibility intervals (CI) as well as expected frequencies of HS-A for selected models and predictor levels. Of n=1933 autopsy participants included (average age at death of 83 years, 51.3% women), HS-A was present in 278 (14.4%). LATE-NC was strongly associated with HS-A (aOR=3.7, 95% CI=[2.8, 5.0]). While ADNC showed a modest association with HS-A in models where LATE-NC was not included as a predictor (aOR=1.4, CI=[1.1, 1.8]), this association was reduced when adjusting for LATE-NC (aOR=1.11, CI=[0.9, 1.5]); results were similar for the ADNC-related A/B/C scores and limbic LBs. However, several cerebrovascular NCs were similarly associated with HS-A both without adjusting for LATE-NC (atherosclerosis aOR=1.4, arteriolosclerosis aOR=1.6, white matter rarefaction (WMR) aOR=1.4) and with adjusting for LATE-NC (atherosclerosis aOR=1.4, arteriolosclerosis aOR=1.5, WMR aOR=1.3). In a combined model, LATE-NC was strongly associated with HS-A, but global cerebrovascular NCs, as well as APOE-ε4 (increased odds), and education (decreased odds), were also associated with HS-A. Predicted HS-A frequency for predictor levels of no LATE-NC or global cerebrovascular NCs was 1.5% (CI=[0.6%, 3.1%]), while it was 94.5% (CI=[84%, 99.5%]) for LATE-NC stage 3 and severe global cerebrovascular NC levels. LATE-NC is likely the most important cause of HS-A. While ADNC seems to be associated with HS-A through its association with LATE-NC, the association of cerebrovascular with HS-A independent of LATE-NC underlines the importance of vascular factors in the etiology of HS-A.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"14 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143910429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}