Brain最新文献

{"title":"Normalization of network activity in an epilepsy model with a constitutively active GABBR2 variant.","authors":"Michal Stawarski,Daniel Ulrich,Sebastian Reinartz,Jochen Schwenk,Li-Yuan Chen,Diego Fernandez-Fernandez,Bartosz Adam Frycz,Mehdi Tafti,Yoon Jeon,Ho Lee,Je Kyung Seong,Murim Choi,Robert Lütjens,Martin Gassmann,Bernd Fakler,Tania Rinaldi Barkat,Bernhard Bettler","doi":"10.1093/brain/awaf356","DOIUrl":"https://doi.org/10.1093/brain/awaf356","url":null,"abstract":"The neurotransmitter GABA activates G protein-coupled GABAB receptors (GBRs) that mediate neuronal inhibition in the brain. These receptors function as obligate heterodimers, consisting of the GB1 and GB2 subunits, with GB1 binding GABA and GB2 interacting with the G protein. The monoallelic variants p.A567T, p.S695I, and p.I705N in the GABBR2 gene, which encodes the GB2 subunit, have been associated with epileptic encephalopathy and Rett-like disorders. The clinical phenotypes overlap with those seen in individuals with monoallelic loss-of-function variants in GABBR1, the gene encoding the GB1 subunit. To investigate the effects of these GABBR2 variants on GBR function, we expressed the variants in heterologous cells and evaluated their pharmacological profiles using a luciferase reporter assay. Furthermore, we introduced the epileptic encephalopathy-associated p.I705N variant into the mouse Gabbr2 gene to examine its impact on neuronal and network activity. These mice were analyzed using proteomic approaches, in combination with in vitro and in vivo electrophysiological techniques. Finally, we evaluated whether the observed network alterations could be reversed pharmacologically. In heterologous cells, all variants displayed strong constitutive activity, reaching 50-100% of the maximal GABA-induced activity of wild-type receptors. This gain-of-function effect was evident regardless of whether the variants were expressed as individual subunits or as heterodimeric receptors. EEG recordings from Gabbr2I704N/+ mice revealed abnormal high-amplitude synchronization in the δ frequency band, without overt seizures. Electrophysiological recordings from brain slices confirmed an increase in constitutive activity in both pre- and postsynaptic GBRs, but also revealed a significant reduction in receptor responsiveness to agonists. Proteomic analysis of brain tissue further revealed a downregulation of both GB1 and GB2 subunits, along with several G protein signaling components. This downregulation likely serves as an adaptive response to the heightened constitutive activity, reducing not only the activity of the variant receptors but also the signaling of wild-type receptors. In vivo recordings from the auditory cortex of awake Gabbr2I704N/+ mice revealed reduced spontaneous neuronal activity and a slower decline in neuronal activity following auditory stimuli. Treatment with a positive allosteric modulator of GBRs normalized spontaneous network activity and the termination of neuronal activity after sensory stimulation in these mice. In conclusion, our findings indicate that the clinical phenotypes associated with constitutively active GABBR2 variants are driven by an adaptive downregulation of GBRs and their key signaling components. Therefore, in monoallelic individuals, positive allosteric modulators that enhance wild-type receptor activity may provide a promising therapeutic strategy.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"57 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145133944","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":"Epilepsy concordance in monozygotic twins: the role of common genetic variants.","authors":"Yew Li Dang,Karen L Oliver,Kate Esnault,Melanie Bahlo,Piero Perucca,Samuel F Berkovic","doi":"10.1093/brain/awaf362","DOIUrl":"https://doi.org/10.1093/brain/awaf362","url":null,"abstract":"Factors underlying discordance for epilepsy in monozygotic twins, in the absence of obvious acquired insults, are incompletely understood. Whilst subtle lesions and postzygotic mutations are sometimes observed, the contribution of common genetic variants remains unexplored. We investigated the role of these variants, measured by polygenic risk scores, in epilepsy concordance. We hypothesized that higher epilepsy polygenic risk scores in concordant monozygotic twins, compared to discordant monozygotic twins and controls, reflect increased epilepsy risk, raising the likelihood of both twins being affected. We calculated epilepsy polygenic risk scores for 102 monozygotic twin pairs (49 concordant, 53 discordant) and 14,632 controls using 2023 epilepsy genome-wide association study summary statistics. Logistic regression, adjusted for sex and principal ancestry components, showed that concordant pairs had significantly higher epilepsy polygenic risk scores than discordant pairs (mean 0.71 vs 0.18; padj=0.03) and controls (mean 0.71 vs 0; padj=0.001). In contrast, epilepsy polygenic risk scores in discordant pairs did not differ from controls (mean 0.18 vs 0; padj=0.38). Our findings suggest that concordance for epilepsy in monozygotic twins is partly driven by common genetic variant burden, underscoring the potential utility of epilepsy polygenic risk scores as predictive markers for epilepsy risk in the general population.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"15 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145133982","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":"Neurofilament light chain as a prognostic marker in cerebral adrenoleukodystrophy.","authors":"Elizabeth I Pierpont,Ashish O Gupta,Julie B Eisengart,Ryan Shanley,Rhys O Evans,Daniel Loes,David Nascene,Srikala Narayanan,Paul J Orchard,Troy C Lund","doi":"10.1093/brain/awaf359","DOIUrl":"https://doi.org/10.1093/brain/awaf359","url":null,"abstract":"Cerebral adrenoleukodystrophy (C-ALD) is a rapidly progressing inflammatory neurodegenerative disease with unpredictable onset in males with ALD. It must be treated at an early stage of demyelination, determined by MRI, to preserve neurocognitive function. Validation of biochemical markers that can aid in prediction of functional outcomes is needed for optimizing disease management and therapeutic development. Our objective was to determine whether plasma neurofilament light chain (NfL), a biomarker of neuroaxonal injury, corresponds to functional outcomes after standard of care treatment with hematopoietic stem cell transplantation (HSCT). This retrospective observational cohort study examined pre-treatment biomarker levels and neurocognitive outcomes 1 year after treatment. Plasma NfL concentrations were measured by SiMoA Assay in 27 patients with C-ALD (mean age: 8.0±2.6 years) at a median of 10 days prior to HSCT. White matter lesions were characterized by Loes MRI severity scores. Following treatment, neurocognitive outcomes across six domains were measured at a median of 1.0 years post-HSCT using the Wechsler intelligence quotient (IQ) scales, the Beery-Buktenica Test of Visual-Motor Integration, and the Purdue Pegboard test. Pre-HSCT NfL values in C-ALD patients ranged from 5.0 to 911.0 pg/mL, with a median of 35.8. Higher NfL levels were associated with lower post-HSCT scores across all neurocognitive domains (p<.05). Large effect sizes were seen for visual reasoning, processing speed, fine motor dexterity, and visual-motor integration (Pearson correlations: r=-0.74 to -0.84). Partial correlations showed a moderate association between NfL and neurocognitive outcomes even when adjusting for MRI severity scores. NfL has a strong correlation with neurocognitive status following treatment for C-ALD. These encouraging findings suggest an opportunity to improve our capacity to forecast outcomes, and therefore improve counseling for families considering cellular therapies.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"89 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127157","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":"Granulocyte and astrocyte markers distinguish MOG-antibody disease and neuromyelitis optica from multiple sclerosis.","authors":"Roberto Furlan,Sabine Schaedelin,Jette Lautrup Frederiksen,Mitsuru Watanabe,Fredrik Piehl,Katharina Fink,Ellen Iacobaeus,Björn Evertsson,Mohsen Khademi,Matteo Gastaldi,Giacomo Greco,Sara Mariotto,Sara Carta,Alessia Di Sapio,Cecilia Irene Bava,Lucia Giorgi,Pascal Benkert,Aleksandra Maleska Maceski,Johanna Oechtering,Eline Willemse,Anne-Katrin Pröbstel,Roxanne Pretzsch,Annamaria Finardi,Alessandra Mandelli,Daniel Anthony,Jens Kuhle,David Leppert","doi":"10.1093/brain/awaf345","DOIUrl":"https://doi.org/10.1093/brain/awaf345","url":null,"abstract":"Granulocytes play a well-established role in the pathogenesis of brain tissue damage in neuromyelitis optica spectrum disorder (NMOSD). The release of granulocyte activation markers (GAM) into CSF has recently been shown to distinguish NMOSD from multiple sclerosis (MS) with high accuracy. However, their pathogenetic role in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is less clear, and their usefulness for diagnostic differentiation is unknown. This observational cohort study by eight tertiary centres in Europe and Japan included 244 CSF samples from patients with MOGAD (n=71), NMOSD (n=48), MS (n=125), and control persons (n=19). CSF levels of GAM (neutrophil elastase, myeloperoxidase, NGAL, MMP-8, MMP-9), astrocyte damage markers (ADM: glial fibrillary acidic protein (GFAP), S100B), and complement factors C5 and C5a were analysed by capillary ELISA (Ella™) or Luminex®. The primary outcome was the capacity of these markers to differentiate MOGAD, NMOSD, and MS in the acute (≤21 days post-exacerbation) stage, and the correlation of GAM with C5 and C5a. Secondary analyses included the correlations of these markers with disability severity, measured by the Expanded Disability Status Scale (EDSS). GAM (except for MMP-9), ADM, and C5/C5a levels peaked at onset of disease exacerbation of MOGAD and NMOSD (regardless of aquaporin-4 antibody status), and were significantly higher than in MS. MMP-9 levels were continuously increased in MS over MOGAD and NMOSD, both in acute and subacute/chronic stages. C5 and C5a were equally increased over MS in acute stages of MOGAD and NMOSD. A logistic model and receiver operating characteristics analyses incorporating GAM and C5 displayed high discriminatory power between MOGAD/NMOSD vs MS (area under the curve (AUC) 0.880), NMOSD vs MS (AUC 0.837), and MOGAD vs MS (AUC 0.925) in acute stages. Accordingly, increased ADM levels in NMOSD differentiated NMOSD from MS and MOGAD (AUC 0.897 and 0.843, respectively). GAM levels correlated with EDSS scores in MOGAD and NMOSD, but not in MS, while those of ADM correlated with disability in NMOSD, but not in MOGAD and MS. Determining CSF levels of GAM and C5/C5a, and of ADM provide a biology-driven approach to differentiate MOGAD, NMOSD and MS. Their measurement can be processed faster and with similar accuracy than with most auto-antibody assays, enabling timely initiation of appropriate therapy in acute presentations. The correlation between GAM and C5/C5a levels with neurological impairment in MOGAD and NMOSD corroborates their role as effectors of neural damage, supporting the acute stage use of inhibitors of C5 activation.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"61 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127158","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":"Enhanced clinical trial stratification in spinal cord injury: the value of electrophysiology","authors":"Paulina S Scheuren, Martin Schubert, Michèle Hubli, Catherine R Jutzeler, Rüdiger Rupp, Rainer Abel, Doris Maier, Klaus Röhl, Michael Baumberger, Margret Hund-Georgiadis, Marion Saur, Jesús Benito-Penalva, Kerstin Rehahn, Mirko Aach, Andreas Badke, Jiri Kriz, Patrick Freund, Norbert Weidner, Martin E Schwab, John L K Kramer, Armin Curt","doi":"10.1093/brain/awaf354","DOIUrl":"https://doi.org/10.1093/brain/awaf354","url":null,"abstract":"There are no approved interventional therapies, aside from neurorehabilitation, that enhance neurological recovery after acute traumatic spinal cord injury (SCI). A key challenge is the lack of biomarkers surpassing clinical standards for optimal stratification. We evaluated electrophysiological markers of preserved neuronal function to improve enrichment stategies over clinical measures. We hypothesized that participants with preserved electrophysiological markers would achieve greater neurological and functional recovery in response to a plasticity-inducing intervention. We conducted a retrospective stratification analysis of data from the recently completed randomized, placebo-controlled, phase-2b Nogo Inhibition in SCI (NISCI) trial (NCT03935321) investigating the efficacy of NG101, a recombinant human antibody that neutralises the neurite outgrowth-inhibiting protein Nogo-A. Participants aged 18–70 years with acute (4 - 28 days) cervical SCI were eligible. At screening, all participants underwent clinical neurological examination and electrophysiological recordings (i.e., somatosensory evoked potentials). Treatment effect sizes for the recovery of upper extremity motor scores and spinal cord independence measure of self-care (6 - months change) between NG101 and placebo groups were compared for stratification based on clinical versus electrophysiological criteria. Power analyses were conducted to estimate the required sample sizes needed for each method. The cohort included 116 participants (45.5 ± 16.8 years, 74 NG101/41 placebo). Clinical stratification showed greater functional recovery in motor-incomplete participants treated with NG101 versus placebo (estimate 0.02 [95%CI: 0.006-0.038], p = 0.007). Electrophysiological stratification revealed greater functional recovery in participants with preserved SSEPs treated with NG101 versus placebo (0.04 [0.015-0.054], p &amp;lt; 0.001). Effect sizes were large for electrophysiological (Cohen’s d = 0.94), but small for clinical stratification (Cohen’s d = 0.46). Power analyses demonstrated smaller required sample sizes for electrophysiological (Nreq= 32) versus clinical stratification (Nreq = 120). This study shows the value of electrophysiology compared to clinical measures for biomarker-driven enrichment and improved power in acute SCI trials. We emphasize the importance of functionally spared neuronal pathways in promoting recovery in response to plasticity-inducing interventions like anti-Nogo-A antibodies.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"14 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145133545","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":"Wherever tau pathology starts, propagation will follow brain connections","authors":"Vincent Malotaux, Yasmine Salman, Bernard J Hanseeuw","doi":"10.1093/brain/awaf350","DOIUrl":"https://doi.org/10.1093/brain/awaf350","url":null,"abstract":"This scientific commentary refers to ‘Connectivity as a universal predictor of tau progression in atypical Alzheimer’s disease’ by de Bruin et al. (https://doi.org/10.1093/brain/awaf279).","PeriodicalId":9063,"journal":{"name":"Brain","volume":"19 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145133577","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 presymptomatic and early manifestations of semantic dementia.","authors":"David J Whiteside,Matthew A Rouse,P Simon Jones,Ian Coyle-Gilchrist,Alexander G Murley,Katherine Stockton,Laura E Hughes,Richard A I Bethlehem,Varun Warrier,Matthew A Lambon Ralph,Timothy Rittman,James B Rowe","doi":"10.1093/brain/awaf351","DOIUrl":"https://doi.org/10.1093/brain/awaf351","url":null,"abstract":"People with semantic dementia (SD) or semantic variant primary progressive aphasia typically present with marked atrophy of the anterior temporal lobe, and thereafter progress more slowly than other forms of frontotemporal dementia. This suggests a prolonged prodromal phase with accumulation of neuropathology and minimal symptoms, about which little is known. To study early and presymptomatic SD, we first examine a well-characterised cohort of people with SD recruited from the Cambridge Centre for Frontotemporal Dementia. Five people with early SD had coincidental MRI prior to the onset of symptoms, or were healthy volunteers in research with anterior temporal lobe atrophy as an incidental finding. We model longitudinal imaging changes in left- and right-lateralised SD to predict atrophy at symptom onset. We then assess 61,203 participants with structural brain MRI in the UK Biobank to find individuals with imaging changes in keeping with SD but with no neurodegenerative diagnosis. To identify these individuals in UK Biobank, we design an ensemble-based classifier, differentiating baseline structural MRI in SD from healthy controls and patients with other neurodegenerative diseases, including other causes of frontotemporal lobar degeneration. We train the classifier on a Cambridge-based cohort (SD n=47, other neurodegenerative diseases n=498, healthy controls n=88) and test it on a combined cohort from the Neuroimaging in Frontotemporal Dementia study and the Alzheimer's Disease Neuroimaging Initiative (SD n=42, other neurodegenerative n=449, healthy control n=127). From our case series, we find people with marked atrophy three to five years before recognition of symptom onset in left- or right-predominant SD. We present right-lateralised cases with subtle multimodal semantic impairment, found concurrently with only mild behavioural disturbance. We show that imaging measures can be used to reliably and accurately differentiate clinical SD from other neurodegenerative diseases (recall 0.88, precision 0.95, F1 score 0.91). We find individuals with no neurodegenerative diagnosis in the UK Biobank with striking left-lateralised (prevalence ages 45-85 4.8/100,000) or right-lateralised (5.9/100,000) anterior temporal lobe atrophy, with deficits on cognitive testing suggestive of semantic impairment. These individuals show progressive involvement of other cognitive domains in longitudinal follow-up. Together, our findings suggest that (i) there is a burden of incipient early anterior temporal lobe atrophy in older populations, with comparable prevalence of left- and right-sided cases from this prospective unbiased approach to identification, (ii) substantial atrophy is required for manifest symptoms, particularly in right-lateralised cases, and (iii) semantic deficits across multiple domains can be detected in the early symptomatic phase.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"26 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127186","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 molecular basis of KCNH1-related epileptic encephalopathy and the challenge of developing targeted therapeutics.","authors":"Alexandra K Sundman,Shuyi Jin,Lata Vadlamudi,Glenn F King","doi":"10.1093/brain/awaf353","DOIUrl":"https://doi.org/10.1093/brain/awaf353","url":null,"abstract":"Epilepsy is a common but heterogenous neurological disorder characterised by recurrent seizures resulting from aberrant hypersynchronous electrical discharges in all or part of the brain. While there are numerous potential causes, such as traumatic brain injury, stroke, and infection, many epilepsies have a genetic basis. Here we review the molecular basis, clinical phenotype and treatment options for KCNH1 epilepsy, which is caused by gain-of-function mutations in the gene KCNH1, which encodes the voltage-gated potassium channel KV10.1. Although first discovered in patients with Temple-Baraitser Syndrome and Zimmermann-Laband Syndrome, these genetic disorders are now recognised as belonging to a broad spectrum of KCNH1-related encephalopathies characterised by developmental delay, intellectual disability, facial dysmorphism, and infantile-onset seizures. A major challenge in developing disease-specific anti-seizure medications for KCNH1 epilepsy is selectivity over KV11.1 (hERG), a closely related channel that plays a fundamental role in repolarisation of the cardiac action potential and which is uniquely susceptible to inhibition by a diverse range of drugs. We argue that allosteric modulators of KV10.1 that induce a depolarising shift in the channel's activation threshold are more likely to be provide seizure control in KCNH1 epilepsy patients than pore blockers that annihilate channel function.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"99 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127160","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":"Covert consciousness: what's in a name?","authors":"Charlène Aubinet,Jan Claassen,Brian L Edlow,David Fischer,Olivia Gosseries,Christof Koch,Daniel Kondziella,Marcello Massimini,Michael J Young","doi":"10.1093/brain/awaf349","DOIUrl":"https://doi.org/10.1093/brain/awaf349","url":null,"abstract":"Over the past decade, it has become apparent that up to 25% of behaviorally unresponsive patients with acute or chronic disorders of consciousness either reveal high spatio-temporal complexity following a direct electrical or magnetic pulse to the brain, or highly differentiated electroencephalographic responses, or can, voluntarily modulate their brain activity on command, each of which has been interpreted, to varying degrees, as evidence of consciousness. Practitioners designate this phenomenon using a dizzying variety of terms. The realization that unresponsiveness does not equate to unconsciousness changes the way patients should be assessed and how the medical team communicates with the patient, their families and the world at large. We here propose that the term covert consciousness be used in all such communications to designate this subcategory of behavioral unresponsive patients, with context-appropriate qualifiers and counseling accompanying its use.","PeriodicalId":9063,"journal":{"name":"Brain","volume":"63 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117059","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":"Lack of statistical significance is not evidence against modularity in visual feature processing.","authors":"Joseph C Griffis,Aaron D Boes","doi":"10.1093/brain/awaf352","DOIUrl":"https://doi.org/10.1093/brain/awaf352","url":null,"abstract":"","PeriodicalId":9063,"journal":{"name":"Brain","volume":"80 1","pages":""},"PeriodicalIF":14.5,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127159","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}