Brain最新文献

{"title":"Beyond human-initiated screening: the imperative for fully autonomous brain health surveillance.","authors":"Neguine Rezaii, Hossein Estiri","doi":"10.1093/brain/awag167","DOIUrl":"https://doi.org/10.1093/brain/awag167","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833273","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":"King's stages of amyotrophic lateral sclerosis: an 18F-FDG-PET study of brain connectivity.","authors":"Francesca Di Pede, Sara Cabras, Umberto Manera, Rosario Vasta, Grazia Zocco, Emilio Minerva, Enrico Matteoni, Filippo De Mattei, Giorgio Pellegrino, Francesca Palumbo, Daniela Pascariu, Stefano Callegaro, Alessandra Maccabeo, Giulia Polverari, Alessio Martino, Alessandro Giuliani, Cristina Moglia, Andrea Calvo, Adriano Chiò, Marco Pagani, Antonio Canosa","doi":"10.1093/brain/awag159","DOIUrl":"https://doi.org/10.1093/brain/awag159","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting upper and lower motor neurons. TDP-43 proteinopathy is the neuropathological signature of the disease, and 18F-FDG-PET serves as a marker of neurodegeneration in vivo. The aim of the present cross-sectional study was to disentangle 18F-FDG-PET correlates of disease severity assessed through the King's staging system, by exploring connectivity changes across motor stages. ALS patients classified as King's stage 1, 2 and 3, who underwent brain 18F-FDG-PET at diagnosis from 2008 to 2022 at the ALS Centre of Turin, were included. A multiple regression analysis to evaluate the relationship between brain metabolism and King's stage was performed. The clusters showing significant results were used as seed regions in an inter-regional correlation analysis (IRCA), performed for each stage. Out of a total of 832 ALS patients, 337 were classified as King's stage 1, 274 as stage 2, and 221 as stage 3. The three groups significantly differed in age at PET, disease duration and total ALSFRS-R score at the time of PET, C9ORF72 status, and the distribution of cognitive categories. We found a decreasing metabolic gradient from King's stage 1 to King's stage 3 in a cluster encompassing motor and cognitive areas. As King's stage increases, we found a decrease of connectivity within the sensorimotor and cognitive areas. The IRCA also showed the connectivity of motor and cognitive regions with temporal and cerebellar regions. The connectivity with temporal regions found in King's stage 1 decreases in King's stage 2 and finally disappears in King's stage 3. The connectivity with the cerebellum occurs in King's stage 2 and decreases in King's stage 3. The changes of connectivity of motor and cognitive areas with temporal and cerebellar regions among different King's stages might reflect the spread of TDP-43 proteinopathy or a compensatory mechanism, respectively. The present study suggests that 18F-FDG-PET imaging of the brain may be integrated with King's staging system to assess the extent of the pathogenic process in the context of clinical trials.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855859","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":"Paediatric functional seizures: when care models meet clinical reality.","authors":"Apurva Parikh, Dara V F Albert, Ilana Yel, Brian Bronson","doi":"10.1093/brain/awag168","DOIUrl":"https://doi.org/10.1093/brain/awag168","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833329","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":"Autologous adipose-derived mesenchymal stromal cells for chronic traumatic brain injury.","authors":"Charles S Cox, Janet R Ashley, Jenifer Juranek, Linda Ewing-Cobbs, Alan R Prossin, Claudia Pedroza, Bingrui Chen, Steven Kosmach, Maria Carmen Duron, Michael C Scott, Joana Bianchi, Aidan Collier, Scott D Olson, Jacob B Schriner, Sean I Savitz","doi":"10.1093/brain/awag165","DOIUrl":"https://doi.org/10.1093/brain/awag165","url":null,"abstract":"<p><p>Secondary injury from traumatic brain injury (TBI) leads to a chronic inflammatory process, neurodegeneration, and tissue loss, resulting in poor outcomes. Mesenchymal stromal cell (MSC) treatment can dampen microglial activation and improve TBI outcomes. Our study aimed to assess the impact of autologous adipose-derived MSC treatment in adult patients with chronic TBI using imaging, functional, and neurocognitive outcome measures. Our Phase 1/2a study analyzed safety and treatment effect of 3 intravenous infusions (over 6 weeks) of autologous adipose-derived MSCs (HB-adMSCs) in 24 chronic TBI patients. Outcome measures included functional, neuropsychological, and psychometric testing; multimodal MRI; and PET using [11C]ER176 to measure brain immune cell density. There were no serious treatment-related adverse events. DT-MRI analyses in a priori regions of interest showed that at 6 months after treatment, elevated mean diffusivity volumes (supraMD) were significantly reduced bilaterally in the hippocampus (mean decrease 163.51 mm3, 95% CI -286.55 to -41.51 mm3; P=0.013). A trend for reduced supraMD was observed in the amygdala (mean decrease 113.60 mm3, 95% CI -229.52 to 2.90 mm3; P=0.058); no changes in the insula were observed (P=0.19). Brain-behavior analyses indicated significant interactions between levels in baseline neuropsychological assessments of anxiety and depression and magnitude of supraMD changes in the amygdala and hippocampus, respectively. Macrostructural volumetric changes were not significant in the hippocampus, amygdala, or insula (all P  >0.10). PET results showed that HB-adMSC treatment induced significant reductions in brain immune cell density in the right caudate (x,y,z: 12,2,7; T20 = 4.1; P <0.0003), extending into both the right ventral anterior thalamus (x,y,z: 13, -2,11; T20 = 3.6; P < 0.0009) and right nucleus accumbens (x,y,z: 8,9, -3; T20 = 2.5; P < 0.01), and right parahippocampal gyrus (x,y,z: 29, -40, -7; T20 = 3.1; P <0.003). Reductions in measures of depression (P=0.026), fatigue (P=0.008), and pain (P=0.007) 6 months after treatment were also observed. Our study demonstrates autologous adipose-derived MSCs for chronic TBI are safe, have clinically relevant treatment effect sizes in functional and neurocognitive outcome measures, yield significant improvements in specified measures of microstructural integrity (i.e., reduced volume of elevated MD voxels) in brain-based behavior relations, and reduce density of brain immune cells in regions corresponding to pain, fatigue, and depression. These data provide quantitative justification for the sample size of next-phase clinical trials using either functional outcomes or surrogate imaging outcomes.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833322","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":"Circular RNA SCMH1 promotes persistent brain repair via N6-methyladenosine methylation post stroke.","authors":"Ying Bai, Ningbo Cai, Liying Wen, Lizhi Pang, Yurui Yang, Ling Shen, Yuan Zhang, Zhuojuan Luo, Jie Chao, Bing Han, Honghong Yao","doi":"10.1093/brain/awag161","DOIUrl":"https://doi.org/10.1093/brain/awag161","url":null,"abstract":"<p><p>Circular RNA (circRNA)-based nucleic acid therapeutics exhibits distinct pharmacological advantages including sustained therapeutic effects from single-dose administration, but the molecular basis governing this persistence remains mechanistically unresolved. Using single-cell RNA sequencing (scRNA-seq), methylated RNA immunoprecipitation sequencing (MeRIP-seq), and genetic animal models, we demonstrated that a single dose of exogenous circSCMH1 sustained elevated endogenous circSCMH1 levels in the peri-infarct region. This persistence stems from a self-sustaining loop initiated by exogenous circSCMH1, as confirmed by experiments with a modified circSCMH1 variant (ΔcircSCMH1), which distinguishes endogenous from exogenous sources. Mechanistically, microglial overexpression of the m6A demethylase FTO enhances circSCMH1 biogenesis by suppressing m6A methylation, with YTHDC1 identified as the primary m6A reader protein facilitating this process. Furthermore, YTHDC1 collaborates with Exportin-4 to mediate m6A-dependent nuclear export of circSCMH1, a step critical for its therapeutic efficacy. In Exportin-4-deficient mice, impaired nuclear export abolishes the sustained brain repair induced by circSCMH1, as evidenced by diminished sensorimotor recovery in behavioural tests. These findings elucidate how a single dose of circSCMH1 improves brain repair through a self-sustaining loop that leverages endogenous circRNA biogenesis machinery. Unlike traditional therapies requiring repeated dosing, this approach achieves prolonged therapeutic efficacy, offering substantial translational advantages for stroke treatment.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833251","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":"Targeting glutamatergic pathways: genetic insights into comorbid neurodevelopmental disorders.","authors":"Joseph T Glessner, Munir E Khan, Xiao Chang, Yichuan Liu, Shahram Torkamandi, Deborah Abrams, F George Otieno, Jihoon Kim, Yeshwanth Mahesh, Maria Lemma, Frank Mentch, Jin Li, Charlly Kao, Michael E March, Huiqi Qu, John Connolly, Hakon Hakonarson","doi":"10.1093/brain/awag152","DOIUrl":"https://doi.org/10.1093/brain/awag152","url":null,"abstract":"<p><p>Copy number variants (CNVs) in genes encoding metabotropic glutamate receptors (GRMs) have been previously implicated in attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). However, investigations of their role in comorbid ADHD patients suffering from coexisting neurodevelopmental disorders (NDDs), such as anxiety and ASD with or without developmental delay remains limited. To assess the enrichment of CNVs in GRM genes and their molecular interaction networks in a large pediatric cohort with ADHD and comorbid NDDs, we analyzed CNV data from 72,626 pediatric participants recruited through the Center for Applied Genomics at Children's Hospital of Philadelphia. The cohort includes 12,472 individuals diagnosed with ADHD (including 7,967 with other NDD comorbid conditions). CNVs were identified using PennCNV and annotated for overlap with GRM genes and their protein-protein interaction (PPI) networks using data from STRING. We evaluated CNV enrichment in ADHD cases with and without comorbid diagnoses, including autism spectrum disorder (ASD), anxiety, and developmental delay. Significant enrichment of CNVs was observed in GRM-interacting networks among ADHD cases with comorbid NDDs. Specifically, 27 genes interacting with primary GRM genes were significantly enriched in CNVs in these individuals with false discovery rate (FDR) < 0.05, compared to ADHD-only cases or disease-free controls. These included key neurodevelopmental genes such as DLG2, NRXN1, SHANK3, and SYNGAP1, which are involved in synaptic signaling and glutamatergic neurotransmission. In contrast, enrichment of GRM network gene CNVs observed in ADHD-only cases was notably less. Our findings support a distinct genetic profile in ADHD cases with comorbid NDDs, marked by CNV enrichment in glutamatergic signaling pathways involving GRM-interacting genes. These results suggest that GRM network disruptions contribute to the complexity of the phenotype spectrum in ADHD patients suffering from comorbid neurodevelopmental phenotypes and highlight a potential pathway for targeted, genetically informed interventions in these patients.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833276","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":"Clinical prognostic indicators in multiple system atrophy.","authors":"Yee Yen Goh, Viorica Chelban, Nirosen Vijiaratnam, Christine Girges, Manmohan Sandhu, Riona Fumi, Patrick W Cullinane, Rahema Mohammad, Michele T Hu, James B Rowe, Nicola Pavese, Neil Archibald, Christopher Kobylecki, Thomas Foltynie, Huw R Morris, Tom Warner, Zane Jaunmuktane, Henry Houlden","doi":"10.1093/brain/awag160","DOIUrl":"https://doi.org/10.1093/brain/awag160","url":null,"abstract":"<p><p>Multiple system atrophy (MSA) is a neurodegenerative condition causing parkinsonism, cerebellar ataxia and/or dysautonomia. Typical survival is between 6-10 years, but some people die before five or after 15 years. This heterogeneity complicates advanced planning and clinical trial stratification. MSA prognostication studies have shown conflicting results, possibly due to diagnostic accuracy or study size. We report results from a study of survival prognostic factors in a cohort of 555 MSA patients (including the largest post-mortem confirmed cohort to date of 254 people) gathered through the Queen Square Brain Bank and the PROSPECT-M-UK multi-centre prospective cohort study. Through PROSPECT-M-UK, 318 clinically diagnosed MSA patients (17 overlapped with the QSBB cohort) were followed up annually over 5 years. The QSBB cohort clinical data was collected through retrospective review of primary and secondary care documentation. Survival analysis was performed using counting process Cox proportionate hazards modelling, Kaplan-Meier log-rank testing and landmark survival analysis to account for guarantee-time bias. Mean onset age in the combined cohort was 58.7±9.0y with median survival of 8.25y (95% CI:7.88-8.63). 28.8% were clinically diagnosed in-life with MSA-P, 23.8% MSA-C, 40.2% mixed and the rest as non-MSA diagnoses. Later disease onset was associated with shorter survival (HR=1.04, P<0.001). The commonest cause of death was respiratory infection (67%) followed by disease related decline (20%). Median survival from indoor wheelchair use, gastrostomy insertion or development of unintelligible speech was consistently <1.5 years (95% CI upper limits<2.4 years), making these reliable late-stage disease markers. Using landmark analysis, at 3 years from onset, negative prognostic factors included recurrent falls, unintelligible speech, use of catheters and of medication for orthostatic hypotension (HR = 1.57, 3.29, 1.76, 3.29;all P<0.05). At 5 years from onset, mobility milestones including walking aid use, outdoor and indoor wheelchair use (HR = 1.70, 1.93, 2.62;all P<0.01) became significant, whilst dysautonomia milestones (catheter and orthostatic support medication use) were no longer significant. Median individual Unified Multiple System Atrophy Rating Scale (UMSARS) progression rate (n=91) was 10.27 (IQR:5.31-14.30) points/year and did not correlate with symptom duration. Higher baseline UMSARS and faster UMSARS progression were negative prognostic factors of survival from baseline review (HR=1.03 and 1.07 respectively, both P<0.001). We show that in-clinic rating scales and clinical milestone assessment can aid MSA prognostication. Importantly, prognostic factors demonstrate time-dependent variability, which may contribute to previous heterogeneity observed in smaller studies. This knowledge is important for patient care and should inform future clinical trial stratification.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833278","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":"Neuroinflammation and neurodegeneration trigger a specific splice form of ribosomal protein S24.","authors":"Srivathsa S Magadi, Maria Jonson, Pablo B Lucena, Michele F Caliandro, Beatriz Almeida, Lorina Bilalli, Dimitri Budinger, Anna Tsoi, Maria Ntzouni, Joseph Agi Maqdissi, Lech Kaczmarczyk, Jente J Zijlstra, Matej Faketija, Matthew Perkins, Gesine Paul, Martin Hallbeck, Martin Ingelsson, Joel C Watts, Nicole Reichenbach, Gabor C Petzold, Rico Schieweck, Michael T Heneka, Walker S Jackson","doi":"10.1093/brain/awag166","DOIUrl":"https://doi.org/10.1093/brain/awag166","url":null,"abstract":"<p><p>Neuroinflammation, particularly that involving reactive microglia, the brain's resident immune cells, is implicated in the pathogenesis of major neurodegenerative diseases (NDs). Multiple studies have reported changes in ribosomal protein (RP) expression during neurodegeneration, but the significance of these changes remains unclear. Ribosomes are evolutionarily conserved protein-synthesizing machines, and although commonly viewed as invariant, accumulating evidence suggests functional ribosome specialization through variation in their protein composition. Among RPs, S24, encoded by RPS24 in humans and Rps24 in mice, is unique as its transcripts undergo alternative splicing to produce protein variants with different C-terminal sequences that are differentially expressed across tissues and cell types. Understanding heterogeneous RP expression patterns across brain regions and cell types could reveal mechanisms underlying selective vulnerability in NDs and provide new biomarkers for neuroinflammatory responses. To identify RP expression patterns across brain regions in neurons, astrocytes, and microglia we analyzed cell type-specific translating mRNAs from mice. To investigate Rps24 isoform-specific expression, we performed cell type-resolved transcript analysis and developed antibodies specific for the S24-PKE protein variant encoded by mRNA isoform Rps24c. We examined Rps24c/S24-PKE expression in brains from mouse models of aging and neurodegeneration, as well as in human postmortem tissue from patients with Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). This work revealed distinct RP expression patterns across brain regions and between neurons, astrocytes, and microglia, including neuron-enriched RPs Rpl13a and Rps10. Analysis of RP paralogs revealed complex expression relationships with their canonical counterparts, suggesting regulated mechanisms for generating heterogeneous ribosomes. Across brain regions and cell types, Rplp0 and Rpl13a, commonly used normalization references, showed heterogeneous expression, raising important methodological considerations for gene expression studies. Rps24 isoforms exhibited striking cell type-specific expression patterns. Rps24c was predominantly expressed in microglia and was increased by neuroinflammation caused by aging, neurodegeneration, or inflammatory chemicals. Using S24-PKE-specific antibodies, we verified increased expression of this protein variant in brains with AD, PD, and HD, and in relevant mouse models. These findings establish heterogeneous RP expression as a feature of brain cell types which may enable cell type-specific translation regulation via specialized ribosomes. This work also identifies Rps24c/S24-PKE as a potential novel marker for neuroinflammation and neurodegeneration and provides new tools for monitoring these responses.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833294","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":"GluN2A-NMDA receptors mediate the effect of BDNF on network hyperexcitability in hippocampal neurons.","authors":"Pasqualino De Luca, Miranda Mele, Francesca Napoli, Philemon Mshelia, Rui O Costa, Carlos B Duarte","doi":"10.1093/brain/awag164","DOIUrl":"https://doi.org/10.1093/brain/awag164","url":null,"abstract":"<p><p>Brain-derived neurotrophic factor (BDNF) modulates synaptic plasticity via activation of TrkB receptors and plays a key role in epileptogenesis, though its molecular mechanisms remain incompletely understood. Here, we examined how BDNF-TrkB signaling regulates synaptic GluN2A-containing NMDA receptors (NMDARs) and impacts network synchronization in cultured hippocampal neurons. BDNF increased synaptic surface expression of GluN2A-NMDARs in rat hippocampal synaptoneurosomes and cultured neurons in a time- and protein synthesis-dependent manner. Mechanistically, we identified a signaling cascade involving hnRNPK, Pyk2, and protein kinase C (PKC) as critical for this effect. Knockdown of hnRNPK or Pyk2, PKC inhibition, or expression of a phosphorylation-deficient Pyk2 mutant prevented BDNF-induced GluN2A synaptic accumulation. Pyk2 phosphorylation at Y402 was required for both basal and BDNF-induced GluN2A expression. Multielectrode array recordings demonstrated that BDNF and GluN2A-NMDARs contribute to enhanced network activity following stimulation. In vivo, BDNF-TrkB signaling mediated increased synaptic GluN2A expression in the hippocampus of rats subjected to the pilocarpine model of temporal lobe epilepsy, confirming a TrkB-dependent mechanism. These findings reveal a BDNF/TrkB-PKC-Pyk2-hnRNPK pathway that regulates GluN2A synaptic expression and neuronal excitability, offering new insights into the molecular basis of synaptic plasticity and epilepsy.</p>","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":""},"PeriodicalIF":11.7,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833331","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 emotional cost of caring: amygdala lesions reduce the aversiveness of affective empathy.","authors":"Sijia Zhao","doi":"10.1093/brain/awag110","DOIUrl":"10.1093/brain/awag110","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":" ","pages":"1433-1434"},"PeriodicalIF":11.7,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509601","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}