Brain最新文献

{"title":"Modelling fragile X-associated neuropsychiatric disorders in young inducible 90CGG premutation mice","authors":"Gürsel Çalışkan, Sara Enrile Lacalle, Emre Kul, Miguel del Ángel, Allison Loaiza Zambrano, Renate Hukema, Mónica Santos, Oliver Stork","doi":"10.1093/brain/awaf203","DOIUrl":"https://doi.org/10.1093/brain/awaf203","url":null,"abstract":"Fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurodegenerative disorder caused by a preCGG repeat expansion in the FMR1 gene. Individuals with the FMR1 premutation often exhibit neuropsychiatric symptoms before FXTAS onset, leading to the identification of fragile X-associated neuropsychiatric disorders (FXAND). Rodent models of FXTAS show motor impairments, pathological intranuclear inclusions, and heightened anxiety. However, the early onset of neuropsychiatric features and underlying mechanisms remain poorly understood. To address the above issues, we used the doxycycline (dox)-inducible 90CGG mouse model, with transgene activation at two developmental stages: adolescence and young adulthood. Mice were evaluated in a behavioural battery to assess anxiety-like behaviour, exploration, and motor coordination and learning. Next, we conducted a combination of ex vivo extracellular local field potential recordings to measure synaptic physiology and oscillatory activity in the limbic system, particularly in the basolateral amygdala (BLA) and ventral hippocampus (vH) regions. Parvalbumin interneurons and intranuclear inclusions in the amygdala and hippocampus were investigated by immunofluorescence, while mass spectrometry and gene set enrichment were used to identify differentially expressed proteins molecular pathways. Adolescent 90CGG mice displayed early-onset hyperactivity, transitioning to heightened anxiety in young adulthood, coinciding with the accumulation of intranuclear inclusions in the BLA and vH. Electrophysiological analysis revealed augmented gamma oscillations in the vH, emerging during adolescence and persisting in young adulthood. These changes correlated with a reduction in parvalbumin interneurons in these regions, and together likely contribute to enhanced BLA excitability and impaired vH plasticity. Finally, proteomic analysis of the vH revealed altered proteins linked to attention deficit hyperactivity disorder in adolescence and anxiety/depression in adulthood, aligning well with behavioural findings. Importantly, these behavioural, electrophysiological, and cellular alterations were reversible upon transgene inactivation. This study reveals a temporal progression of CGG premutation effects on behaviour, from hyperactivity to heightened anxiety to late onset motor dysfunction. Moreover, these findings provide altered network activity in the limbic system as a putative mechanism in neuropsychiatric features of premutation carriers.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"38 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201972","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":"PACAP and migraine","authors":"Hans Christoph Diener","doi":"10.1093/brain/awaf131","DOIUrl":"https://doi.org/10.1093/brain/awaf131","url":null,"abstract":"A number of neuropeptides including pituitary adenylate cyclase-activating polypeptide (PACAP) play an important role in the pathophysiology of migraine. Infusions of PACAP in patients with migraine can provoked migraine attacks. A placebo-controlled study with a monoclonal antibody directed against the PACAP-receptor failed to show efficacy. In a small, short, proof of concept study a monoclonal antibody directed against PACAP (Lu AG09222) showed efficacy in the reduction of monthly migraine days compared to placebo, but failed for the endpoint 50%-reduction in migraine days. The ongoing PROCEED-study is a double-blind, placebo-controlled, dose-finding study investigating four different doses of Lu AG09222 vs placebo for migraine prevention is expected to complete in the second half of 2025.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"36 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176598","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":"Correction to: Toxic effects of mutant huntingtin in axons are mediated by its proline-rich domain.","authors":"","doi":"10.1093/brain/awaf189","DOIUrl":"https://doi.org/10.1093/brain/awaf189","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172620","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":"CSF proteomics of semorinemab Alzheimer’s disease trials identifies cell-type specific signatures","authors":"Alyaa M Abdel-Haleem, Ellen Casavant, Balazs Toth, Edmond Teng, Cecilia Monteiro, Nikhil J Pandya, Caspar Glock, Casper C Hoogenraad, Brad A Friedman, Felix L Yeh, Veronica G Anania, Gloriia Novikova","doi":"10.1093/brain/awaf200","DOIUrl":"https://doi.org/10.1093/brain/awaf200","url":null,"abstract":"Targeting of tau pathology has long been proposed as a potential therapeutic strategy for Alzheimer’s disease (AD). Semorinemab is a humanized IgG4 monoclonal antibody that binds to all known isoforms of full-length tau with high affinity and specificity. Semorinemab’s safety and efficacy have been studied in two Phase 2 randomized, double-blind, placebo-controlled, parallel-group clinical trials: Tauriel (prodromal-to-mild AD; NCT03289143; in which semorinemab failed to demonstrate clinical efficacy) and Lauriet (mild-to-moderate AD; NCT03828747. However, semorinemab was associated with a significant slowing in progression in a co-primary endpoint of cognition only in Lauriet but not in Tauriel. Proteomic profiling of CSF collected in these trials was performed to gain a better understanding of the effect of semorinemab in light of the different clinical outcomes. CSF was collected from a subset of patients at baseline and after 49 or 73 weeks in Tauriel and baseline and after 49 or 61 weeks in Lauriet. Samples were analyzed using single-shot FAIMS-DIA-MS and analyzed with Spectronaut and MS Stats. Proteomics results were integrated with publicly available single-nucleus brain datasets to contextualize cellular expression profiles of differentially expressed proteins. A novel proteomics dataset was generated using more than 250 cerebrospinal fluid (CSF) samples where more than 3500 proteins were detected. Treatment-associated proteomic signatures were defined for each clinical trial as the set of proteins significantly elevated in the treatment arm in the respective trial. Integration of the corresponding gene signatures with brain single-nucleus RNA-seq datasets from AD and healthy age-matched controls revealed that the Lauriet signature genes were enriched in microglia, while Tauriel signature genes were more broadly expressed across brain cell types. Furthermore, the Lauriet gene signature was significantly upregulated in microglia from AD patients compared to non-demented controls. The elevation of proteins such as CHI3L1 and GPNMB with treatment suggested an activated glial state. This study demonstrates the utility of CSF clinical proteomics to assess the pharmacodynamic response of semorinemab and contributes to our understanding of how an anti-tau antibody influences disease-relevant pathophysiology in AD.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"87 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144165307","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":"Anatomical progression of genetic frontotemporal lobar degeneration across the lifespan.","authors":"Vincent Planche, Boris Mansencal, Vladimir Fonov, José V Manjon, Thomas Tourdias, 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, Caroline Graff, Daniela Galimberti, Rik Vandenberghe, Alexandre de Mendonça, Pietro Tiraboschi, Isabel Santana, Alexander Gerhard, Johannes Levin, Sandro Sorbi, Markus Otto, Maxime Bertoux, Thibaud Lebouvier, Chris R Butler, Isabelle Le Ber, Elizabeth Finger, Maria Carmela Tartaglia, Mario Masellis, James B Rowe, Matthis Synofzik, Fermin Moreno, Barbara Borroni, Jonathan D Rohrer, D Louis Collins, Simon Ducharme, Pierrick Coupé","doi":"10.1093/brain/awaf195","DOIUrl":"10.1093/brain/awaf195","url":null,"abstract":"<p><p>The recent development of brain charts for the human lifespan offers an ideal modeling framework for pathologies such as genetic frontotemporal lobar degeneration (FTLD) which likely involve both neurodevelopmental and neurodegenerative processes over a lifetime. We have therefore combined this new methodological approach with MRI data from asymptomatic and symptomatic subjects, carrying C9orf72, MAPT or GRN mutations from the GENFI and ALLFTD cohorts. We analyzed 37,532 MRIs from control subjects covering the entire lifespan and a total of 1,341 MRIs from subjects with a pathogenic FTLD mutation, aged from 18 to 86 years old. We detected the first significant regional brain volume differences on average at 27 years old in C9orf72 and MAPT mutation carriers, and at 42 years old in GRN mutation carriers. The delay between the onset of anatomical changes and the average age of symptom onset (i.e. the presymptomatic phase) was 13 years for MAPT, 17 years for GRN, and 34 years for C9orf72 mutation carriers. In terms of effect size, cumulative atrophy over the lifespan was twice as severe in affected brain regions in MAPT than in GRN or C9orf72 mutation carriers. However, the neurodegenerative process was spatially more extensive in C9orf72 (35 brain regions affected out of the 61 tested) compared to GRN or MAPT mutations carriers (25 and 18 regions, respectively). Schematically, the chronological staging of atrophy progression showed an initial involvement of the thalamus in C9orf72 expansion carriers, followed by the fronto-temporo-insular regions, the striatum and the amygdala. In GRN mutation carriers, atrophy began in fronto-insular areas, before progressing toward subcortical structures. In MAPT mutation carriers, atrophy affected the anterior temporal pole with the amygdala and hippocampus, before progressing to fronto-insular regions and the striatum. Our results using brain charts for the human lifespan show that C9orf72 is the most diffuse but also the slowest to emerge among genetic FTLD. MAPT FTLD is more aggressive and focal, while GRN FTLD is also rapidly progressive but with a later onset of the presymptomatic phase. Beyond quantification of the anatomical progression of genetic FTLD over the lifespan, these results may help determine the best timing to model and test disease-modifying strategies in FTLD, and monitor their effect in future clinical trials.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155926","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":"Mapping the peripheral immune landscape of Parkinson's disease patients with single-cell sequencing.","authors":"Gael Moquin-Beaudry, Lovatiana Andriamboavonjy, Sebastien Audet, Laura K Hamilton, Antoine Duquette, Sylvain Chouinard, Michel Panisset, Martine Tetreault","doi":"10.1093/brain/awaf066","DOIUrl":"https://doi.org/10.1093/brain/awaf066","url":null,"abstract":"<p><p>Parkinson's disease is most recognized for its impact on the CNS. However, recent breakthroughs underscore the crucial role of interactions between central and peripheral systems in Parkinson's disease pathogenesis. The spotlight is now shifting as we explore beyond the CNS, discovering that peripheral changes such as inflammatory dysfunctions may predict the rate of disease progression and severity. Despite more than 200 years of research on Parkinson's disease, reliable diagnostic or progression biomarkers and effective disease-modifying treatments are still lacking. Additionally, the cellular mechanisms that drive changes in immunity are largely unknown. Thus, understanding peripheral immune signatures could lead to earlier diagnosis and more effective treatments for Parkinson's disease. Here, we sought to define the transcriptomic alterations of the complete peripheral immune cell compartment by single-cell RNA and T-cell-receptor sequencing with hopes of uncovering Parkinson's disease signatures and potential peripheral blood biomarkers. Following transcriptional profiling of 78 876 cells from 10 healthy controls and 14 Parkinson's disease donors, we observed all expected major classes of immune cells; the myeloid (monocytes, dendritic cells) and lymphoid (T lymphocytes, B lymphocytes, natural killer) compartments were further analysed through bioinformatics re-clustering to obtain the final 38 cellular subtypes. Comparing immune cell subtypes and phenotypes between patients with Parkinson's disease and healthy control subjects revealed notable features of Parkinson's disease: (i) a significant shift of classical CD14+ monocytes towards an activated CD14+/CD83+ state; (ii) changes in lymphocyte subtype abundance, including a significant decrease in CD4+ naive and mucosal-associated invariant T-cell subtypes, along with an increase in CD56+ natural killer cells; (iii) the identification of several specific T-cell clones shared between multiple patients, suggesting the implication of common epitopes in Parkinson's disease pathogenesis; and (iv) a notable increase in the expression of activation signature genes, including the AP-1 stress-response transcription factor complex, across all Parkinson's disease cell types. This signal was not present in atypical parkinsonism patients with multiple system atrophy or progressive supranuclear palsy. Overall, we present a comprehensive atlas of peripheral blood mononuclear cells from healthy and Parkinson's disease donors which should serve as a tool to improve our understanding of the role the immune cell landscape plays in Parkinson's disease pathogenesis.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":10.6,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141430","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 basal forebrain degeneration in isolated REM sleep behaviour disorder","authors":"Ryul Kim, Bora Jin, Heejung Kim, Kyung Ah Woo, Eun Jin Yoon, Seoyeon Kim, Jung Hwan Shin, Hyunwoo Nam, Yu Kyeong Kim, Beomseok Jeon, Jee-Young Lee","doi":"10.1093/brain/awaf196","DOIUrl":"https://doi.org/10.1093/brain/awaf196","url":null,"abstract":"Although growing evidence suggests that cholinergic basal forebrain degeneration is linked to cognitive impairment and axial motor symptoms in Lewy body disorders (LBDs), the cholinergic contribution to their prodromal phase remains largely unknown. Herein, we aimed to address three important yet unresolved questions focusing on prodromal LBDs: (1) to examine whether and where basal forebrain degeneration begins; (2) to determine how such alterations are related to other brain morphometric changes and monoaminergic deficits; and (3) to investigate the extent to which basal forebrain atrophy contributes to the clinical picture. We included 93 patients with polysomnography-confirmed isolated REM sleep behavior disorder (iRBD), 33 with de novo Parkinson’s disease (PD) with a premorbid history of RBD (dnPDRBD), and 36 healthy controls. Participants underwent baseline assessments including volumetric MRI, 18F-FP-CIT PET scan, the Movement Disorders Society-Unified Parkinson's Disease Rating Scale, and neuropsychological evaluations. Regional volumes of cholinergic nuclei 1, 2, and 3 (Ch1–3) and cholinergic nucleus 4 (Ch4) were extracted using probabilistic maps, and voxel-based and surface-based morphometric analyses were applied to identify basal forebrain atrophy-associated cortical and subcortical regions. Subgroups of patients with iRBD underwent repeated motor and cognitive assessments (38 and 34 patients for 2 and 4 years, respectively). Among the basal forebrain complex, Ch4 volumes, but not Ch1–3 volumes, were significantly reduced in patients with iRBD. This reduction positively correlated with limbic regions, including the amygdala and cingulate cortex, and, to a lesser extent, with the neocortical regions, particularly the frontal and temporal cortices. With respect to clinical symptoms, both Ch1–3 and Ch4 volume reductions were modestly associated with severe axial motor symptoms. Additionally, Ch1–3 volume reduction was associated with higher incidence of dementia and faster progression of memory impairment, whereas Ch4 volume reduction was associated with faster progression of limb bradykinesia. Using a multimodal imaging approach, we found that iRBD patients who later converted to PD showed predominant monoaminergic deficits but variable cholinergic involvement, and these patterns were similar to those observed in the dnPDRBD group. Conversely, iRBD patients who later converted to dementia with Lewy bodies showed predominant cholinergic deficits but variable monoaminergic involvement. This comprehensive analysis provides important implications for understanding how cholinergic basal forebrain degeneration is associated with brain morphometric changes, clinical outcomes, and monoaminergic degeneration during the prodromal phase of LBDs.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"25 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136758","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":"SLC35A2 loss-of-function variants affect glycomic signatures, neuronal fate and network dynamics","authors":"Dulcie Lai, Paulina Sosicka, Damian J Williams, MaryAnn E Bowyer, Andrew K Ressler, Sarah E Kohrt, Savannah J Muron, Peter B Crino, Hudson H Freeze, Michael J Boland, Erin L Heinzen","doi":"10.1093/brain/awaf198","DOIUrl":"https://doi.org/10.1093/brain/awaf198","url":null,"abstract":"SLC35A2 encodes a UDP-galactose transporter essential for glycosylation of proteins and galactosylation of lipids and glycosaminoglycans. Germline genetic SLC35A2 variants have been identified in congenital disorders of glycosylation and somatic SLC35A2 variants have been linked to intractable epilepsy associated with malformations of cortical development. However, the functional consequences of these pathogenic variants on brain development and network integrity remain unknown. In this study, we use an isogenic human induced pluripotent stem cell-derived neuron model to comprehensively interrogate the functional impact of loss of function variants in SLC35A2 through the integration of cellular and molecular biology, protein glycosylation analysis, neural network dynamics, and single cell electrophysiology. We show that loss of function variants in SLC35A2 result in disrupted glycomic signatures and precocious neurodevelopment, yielding hypoactive, asynchronous neural networks. This aberrant network activity is attributed to an inhibitory/excitatory imbalance as characterization of neural composition revealed preferential differentiation of SLC35A2 loss of function variants towards the GABAergic fate. Furthermore, electrophysiological recordings of synaptic activity and gene expression differences suggest network phenotypes are driven by changes occurring at the synapse. Our study is the first to provide mechanistic insight regarding the early development and functional connectivity of SLC35A2 loss-of-function variant harboring human neurons, providing important groundwork for future exploration of potential therapeutic interventions.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"23 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144145792","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":"Oligoadenylate synthetase 1a suppresses prion infection through binding to cellular prion protein.","authors":"Takujiro Homma,Takehiro Nakagaki,Takuya Nishinakagawa,Yurie Morita,Ryuichiro Atarashi,Shigeru Kakuta,Yoichiro Iwakura,Noriyuki Nishida,Daisuke Ishibashi","doi":"10.1093/brain/awaf193","DOIUrl":"https://doi.org/10.1093/brain/awaf193","url":null,"abstract":"Prion diseases are fatal neurodegenerative disorders caused by misfolding of the normal prion protein (PrPC) into its infectious β-sheet-rich isoform (PrPSc). Conventionally, prions were thought to be incapable of eliciting robust immune responses because PrPC and PrPSc share an identical primary structure. However, recent evidence highlights the critical involvement of type I interferon (I-IFN) signaling in host defense against prion propagation. Although we have previously shown that I-IFN, activated by interferon regulatory factor 3 (IRF3), plays an essential role in limiting prion invasion, the precise mechanisms underlying its protective effects remain unclear. Here, using in vivo and ex vivo prion infection models, we discovered that 2'-5' oligoadenylate synthetase 1a (Oas1a), an interferon-stimulated gene downstream of the I-IFN receptor, inhibits prion invasion at an early stage. Using Oas1a-knockout mice, we show that loss of Oas1a significantly accelerates prion disease progression and shortens survival, demonstrating its protective role in vivo. Consistent with this, mouse embryonic fibroblasts from Oas1a-knockout mice exhibited significantly increased susceptibility to 22L prion infection, effectively abrogating the anti-prion effects of I-IFN treatment. In addition, we found that recombinant Oas1a, when applied extracellularly, inhibited prion propagation without activating conventional RNase L pathways. Mechanistically, Oas1a directly binds PrPC, preventing its conversion to PrPSc and thus limiting PrPSc accumulation in vitro. These findings highlight the critical role of the IFN-Oas1a axis in limiting prion propagation and underscore its potential as a novel therapeutic target for prion diseases.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"44 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144122188","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":"Models of autoantibody mediated diseases: actively nearing the human gold standard.","authors":"Sarosh R Irani","doi":"10.1093/brain/awaf160","DOIUrl":"https://doi.org/10.1093/brain/awaf160","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":"31 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144122189","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}