Brain communications最新文献

{"title":"Muscle-driven spinal cord histological and transcriptomic alterations in a myotonic dystrophy mouse model: insights into neuropathy.","authors":"Guanzhong Shi, Yining Luan, Yuzhen Ouyang, Kangzhi Chen, Kaiyue Zhang, Zeyi Wen, Huan Yang, Kun Huang","doi":"10.1093/braincomms/fcaf313","DOIUrl":"10.1093/braincomms/fcaf313","url":null,"abstract":"<p><p>Myotonic dystrophy type 1 (DM1) is an inherited neuromuscular disorder characterized by muscle weakness, atrophy and myotonia, with multi-system involvement. Recent studies have highlighted the pathological heterogeneity within the CNS of DM1 patients, particularly significant changes in spinal transcriptome expression and alternative splicing. In this study, we conducted a comprehensive transcriptome analysis of the spinal cord in the muscle-specific DM1 mouse model and their wild-type controls across different life stages: young, adult and old age. Our results revealed an age-dependent increase in differential gene expression between DM1 and wild-type mice with a predominance of downregulated genes. Notably, five genes (<i>Adgre1</i>, <i>Ccl3</i>, <i>Fcrls</i>, <i>Ogfrl1</i> and <i>Reg3b</i>) were consistently differentially expressed across all age groups. We also generated a temporal profile of cell-type proportions and observed reductions in microglia and astrocytes, along with a trend towards increased ventral neuron populations. Additionally, we characterized the temporal splicing alterations in the spinal cord of DM1 mice and compared with homologous exon skipping events in the CNS of DM1 patients. Our RNA sequencing data elucidate the molecular and cellular adaptations of the spinal cord to muscle defects over time, underscoring that splicing abnormalities observed in the CNS of DM1 patients may reflect contributions from muscle pathology. These findings highlight the necessity of a holistic approach to comprehensively understand the complexity of DM1.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf313"},"PeriodicalIF":4.5,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12409276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does p-tau217 play a physiological reparative role in neonates and neurodegenerative diseases?","authors":"Timothy Daly, Lorenzo Pini, Bruno P Imbimbo","doi":"10.1093/braincomms/fcaf321","DOIUrl":"10.1093/braincomms/fcaf321","url":null,"abstract":"","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf321"},"PeriodicalIF":4.5,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12412211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving diagnostic accuracy of routine EEG for epilepsy using deep learning.","authors":"Émile Lemoine, Denahin Toffa, An Qi Xu, Jean-Daniel Tessier, Mezen Jemel, Frédéric Lesage, Dang Khoa Nguyen, Elie Bou Assi","doi":"10.1093/braincomms/fcaf319","DOIUrl":"10.1093/braincomms/fcaf319","url":null,"abstract":"<p><p>The yield of routine EEG to diagnose epilepsy is limited by low sensitivity and the potential for misinterpretation of interictal epileptiform discharges. Our objective is to develop, train and validate a deep learning model that can identify epilepsy from routine EEG recordings, complementing traditional interpretation based on identifying interictal discharges. This is a retrospective cohort study of diagnostic accuracy. All consecutive patients undergoing routine EEG at our tertiary care centre between January 2018 and September 2019 were included. EEGs recorded between July 2019 and September 2019 constituted a temporally shifted testing cohort. The diagnosis of epilepsy was established by the treating neurologist at the end of the available follow-up period, based on clinical file review. Original EEG reports were reviewed for IEDs. We developed seven novel deep learning models based on Vision Transformers and Convolutional Neural Networks, training them to classify raw EEG recordings. We compared their performance to interictal discharge-based interpretation and two previously proposed machine learning methods. The study included 948 EEGs from 846 patients (820 EEGs/728 patients in training/validation, 128 EEGs/118 patients in testing). Median follow-up was 2.2 years and 1.7 years in each cohort, respectively. Our flagship Vision Transformer model, DeepEpilepsy, achieved an area under the receiver operating characteristic curve of 0.76 (95% confidence interval: 0.69-0.83), outperforming interictal discharge-based interpretation (0.69; 0.64-0.73) and previous methods. Combining DeepEpilepsy with interictal discharges increased the performance to 0.83 (0.77-0.89). DeepEpilepsy can identify epilepsy on routine EEG independently of interictal discharges, suggesting that deep learning can detect novel EEG patterns relevant to epilepsy diagnosis. Further research is needed to understand the exact nature of these patterns and evaluate the clinical impact of this increased diagnostic yield in specific settings.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf319"},"PeriodicalIF":4.5,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12419360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paired blood and brain tissue methylation biomarkers in focal cortical dysplasia.","authors":"Ishant Khurana, Jean Khoury, Robyn M Busch, Ingmar Blümcke, Imad Najm, Assam El-Osta","doi":"10.1093/braincomms/fcaf277","DOIUrl":"10.1093/braincomms/fcaf277","url":null,"abstract":"<p><p>Focal Cortical Dysplasia (FCD) is a common cause of drug-resistant epilepsy. These abnormalities arise during embryonic development and are challenging to classify due to their complex nature. The most recent classification update of FCD incorporates genetic and epigenetic results with other clinical data for the management of epilepsy associated with these lesions. Mutations in the mechanistic target of rapamycin pathway have been described in subtypes IIa and IIb of FCD. In this study, we aimed to study brain DNA methylation in human FCD samples and determine whether blood DNA methylation reflects epigenetic changes observed in brain tissue. We studied genome-wide methylation in 21 brain tissue samples (FCD; <i>n =</i> 13 and other pathologies; <i>n =</i> 8) resected from patients with medically intractable epilepsy along with matched blood samples from the same patients. These results were validated with 32 brain-blood matched samples. This study identified both unique and shared methylation signatures in brain and blood for FCD subty pes IIa and IIb and validated three methylation biomarkers (<i>Interleukin-1 receptor accessory protein</i>, <i>Homeodomain-interacting protein kinase 2</i>, and <i>Chronomodulin</i>) that differentiate these subtypes. Methyl-Binding Domain capture sequencing identified 676 551 methylated regions, covering 70% of cytosine-guanine dinucleotide sites in the genome. Adjustments for factors like age, gender, and disease duration were made before analysis. A total of 13 methylation biomarkers were identified for improved classification of FCD IIb from IIa. The three biomarkers showed high specificity and sensitivity, with an area under the curve score of 0.98 and <i>P</i>-value = 0.01. The study highlights the potential use of DNA methylation biomarkers as a non-invasive diagnostic tool for distinguishing between FCD subtypes, which could lead to more accurate treatment decisions for patients with epilepsy. The findings also underscore the importance of methylation patterns in understanding the pathophysiology of FCD.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 4","pages":"fcaf277"},"PeriodicalIF":4.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12371190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative analysis of aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies titres: correlation with relapses.","authors":"Martina Nasello, Mark Woodhall, Huiru Xue, Victor Mgbachi, Ruth Geraldes, Maria Isabel Leite, Patrick Waters, Jacqueline Palace","doi":"10.1093/braincomms/fcaf312","DOIUrl":"10.1093/braincomms/fcaf312","url":null,"abstract":"<p><p>Detection of antibodies against aquaporin-4 (AQP4-IgG) and myelin oligodendrocyte glycoprotein (MOG-IgG) is essential for diagnosis of AQP4-IgG+ neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease. Uncertainties persist regarding the clinical significance of serum antibody titres to predict relapses. We aimed to analyse the trend of serum AQP4-IgG and myelin oligodendrocyte glycoprotein antibody-IgG titres during relapses and periods of clinical stability. In this retrospective study we analysed serum AQP4-IgG and myelin oligodendrocyte glycoprotein antibody -IgG titres from live cell-based assays from the Oxford Autoimmune Neurology Diagnostic Laboratory for the UK specialist NMO Service between February 2010 and June 2024. We recruited seropositive AQP4-neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease patients with serum samples available within 30 days of an attack ('attack') and at least one another sample for comparison within 1 year ('pre-attack' and 'post-attack'). Up to 3 further serum samples were selected within 2, 3 or 4 years after the attack. 117 attacks in 92 AQP4-IgG+ patients (81.5% female) and 127 attacks in 111 myelin oligodendrocyte glycoprotein antibody-IgG+ patients (62.2% female) had appropriate samples. Antibody titres significantly increased from 'pre-attack' to 'attack', decreased from 'attack' to 'post-attack', and remained stable from 2 to 4 years after attacks. Long-term immunosuppressant treatments induced a further decrease in titres during remission in both cohorts. In 40% of samples in both groups there was an increase in titre at relapse. A ≥ 2-fold increase in AQP4-IgG titres had an Odds Ratio (OR) of 6.59% and 91.5% specificity of being associated with a relapse, in myelin oligodendrocyte glycoprotein antibody-IgG+ an OR of 4.87% and 88.6% specificity. 29% (26/92) AQP4-IgG+ patients became 'seronegative' during follow: most patients (64%) had low attack titres (≤100), and the time to seroreversion related the attack titre. In contrast, 41% (46/111) myelin oligodendrocyte glycoprotein antibody-IgG+ patients became 'seronegative', mostly within the first year after the attack regardless of attack titre. In conclusion, in 60% of longitudinal serum samples from patients with AQP4-IgG or myelin oligodendrocyte glycoprotein antibody-IgG there is no increase in antibody titre. When there is an increase, it is most often at relapse. A ≥ 2-fold increase in titres should be a risk particularly in case of treatment de-escalation, non-adherence to treatment or if a pseudo-relapse is suspected.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf312"},"PeriodicalIF":4.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12418092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Skull-meninges-brain connectivity and extra-axial brain tumours.","authors":"Abdurrahman I Islim, Alexandros Vyziotis, Omar N Pathmanaban, David J Coope, Andrew T King, David Brough, Laura Jardine, Kevin N Couper, Andrew D Greenhalgh","doi":"10.1093/braincomms/fcaf311","DOIUrl":"10.1093/braincomms/fcaf311","url":null,"abstract":"<p><p>The cortex of the brain is covered by three meningeal layers: the dura, the arachnoid, and the pia mater. Substantial discoveries have been made demonstrating the structural and functional relationships between these layers, and with other neighbouring structures such as the skull. Importantly, improved understanding of the meningeal lymphatic network places the meninges at the nexus of a cross talk between the brain, peripheral immune system, and the skull bone marrow. The meningeal lymphatic network has been shown to regulate immune responses in models of health and disease states, such as intra-axial brain tumours, affecting a tumour's behaviour. Unsurprisingly, a diverse array of resident and circulating immune cells such as macrophages, T-cells and B-cells can be found in the meninges, with specialized organizations or hubs surrounding the dural venous sinuses and cranial nerves. Meningioma and vestibular schwannoma are the most common extra-axial brain tumours, with varying clinical courses related to their immune microenvironments. These tumours commonly occur in proximity to the immune hubs of the meninges. This could point towards a possible bidirectional interaction, not only implicated in regulating tumour immune cell infiltration, but also meningeal inflammation and symptoms such as headaches and anxiety. This review will summarize the meningeal structure and function and highlight how these may be linked to patients with meningioma or vestibular schwannoma.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf311"},"PeriodicalIF":4.5,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12416566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent progression independent of relapse activity in multiple sclerosis.","authors":"Chao Zhu, Zhen Zhou, Tomas Kalincik, Izanne Roos, Katherine Buzzard, Olga Skibina, Raed Alroughani, Jens Kuhle, Marc Girard, Pierre Grammond, Jeannette Lechner-Scott, Oliver Gerlach, Nevin John, Pamela McCombe, Richard Macdonell, Vincent van Pesch, Guy Laureys, Julie Prevost, Dana Horakova, Eva Kubala Havrdova, Tamara Castillo-Triviño, Cristina Ramo-Tello, Yolanda Blanco, Jose E Meca-Lallana, Alessandra Lugaresi, Valentina Tomassini, Elisabetta Cartechini, Maria Pia Amato, Daniele Spitaleri, Francesco Patti, Davide Maimone, Matteo Foschi, Andrea Surcinelli, Emanuele D'Amico, Bassem Yamout, Samia J Khoury, Maria Jose Sa, Cavit Boz, Serkan Ozakbas, Bianca Weinstock-Guttman, Daniel Merlo, Mastura Monif, Vilija G Jokubaitis, Anneke van der Walt, Helmut Butzkueven","doi":"10.1093/braincomms/fcaf306","DOIUrl":"10.1093/braincomms/fcaf306","url":null,"abstract":"<p><p>Patients with relapsing-remitting multiple sclerosis (RRMS) may experience disability progression independent of relapse activity (PIRA), which can be an early sign of secondary progressive MS (SPMS). We defined persistent PIRA as ongoing sustained disability over the entire available follow-up period. However, PIRA events can regress over time. Identifying factors that predict PIRA persistence is of great interest as they can refine the definition of RRMS to SPMS transition. Equally, factors associated with the non-persistence of PIRA have potential treatment implications for patients suffering from a PIRA event. We conducted a study to examine risk factors for PIRA persistence and risk differences in long-term disability progression between persistent and non-persistent PIRA. In this cohort study, we included only patients who had already experienced a PIRA event and investigated the persistence of disability progression following their first PIRA event. Therefore, PIRA occurrence time was set as the baseline. Data were collected from the MSBase registry between April 1995 and January 2024, with a median follow-up of 8.7 years. The primary outcome was time to 6-month confirmed non-persistence of PIRA. Secondary outcomes comprised time to 6-month confirmed Expanded Disability Status Scale (EDSS) 6 and time to SPMS. A stratified Cox regression model was used to identify risk factors associated with non-persistent PIRA. We then matched persistent PIRA patients with non-persistent PIRA patients in a 1:1 ratio using propensity scores, and compared their risk of reaching EDSS 6 using the Cox regression model. We re-matched patients with complete Kurtzke Functional Systems Scores to compare their risks of reaching SPMS. We included 4713 RRMS patients with PIRA, of whom around one-third experienced a post-PIRA disability improvement, over a relatively long period (median of 2.6 years to improvement). Use of high-efficacy disease-modifying therapies (DMT) at baseline [hazard ratio, 1.22; 95% confidence interval, (1.08-1.38); <i>P</i> = 0.0015], lower baseline EDSS [hazard ratio, 0.73 (0.69-0.78); <i>P</i> < 0.0001] and younger age [per 10 years; hazard ratio, 0.84 (0.80-0.89); <i>P</i> < 0.0001] were associated with non-persistent PIRA. Patients with non-persistent PIRA had a hazard ratio of 0.19 [95% confidence interval, (0.15-0.25); <i>P</i> < 0.0001] for reaching EDSS 6 and 0.18 [(0.11-0.29); <i>P</i> < 0.0001] for reaching SPMS compared to patients with persistent PIRA. PIRA events slowly regress in one-third of patients. Patients with persistent PIRA had a substantially higher risk of reaching EDSS 6 and SPMS than those with non-persistent PIRA. Younger age, lower baseline EDSS, and use of high-efficacy DMT during PIRA events were associated with PIRA regression.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf306"},"PeriodicalIF":4.5,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12405762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145002110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detection of cognitive deficits years prior to clinical diagnosis across neurological conditions.","authors":"Xin You Tai, Sofia Toniolo, David J Llewellyn, Cornelia M van Duijn, Masud Husain, Sanjay G Manohar","doi":"10.1093/braincomms/fcaf307","DOIUrl":"10.1093/braincomms/fcaf307","url":null,"abstract":"<p><p>Understanding the cognitive trajectory of a neurological disease can provide important insight on underlying mechanisms and disease progression. Cognitive impairment is now well established as beginning many years before the diagnosis of Alzheimer's disease, but pre-diagnostic profiles are unclear for other neurological conditions that may be associated with cognitive impairment. We analysed data from the prospective UK Biobank cohort with study baseline assessment performed between 2006 and 2010 and participants followed until 2021. We examined data from 497 252 participants, aged between 38 and 72 years at baseline, with an imaging sub-sample of 42 468 participants. Using time-to-diagnosis and time-from-diagnosis data in relation to time of assessment, we compared a continuous measure of executive function and magnetic resonance imaging brain measures of total grey matter (GM) and hippocampal volume in individuals with ischaemic stroke, focal epilepsy, Parkinson's disease, multiple sclerosis, motor neurone disease (amyotrophic lateral sclerosis) and migraine. Of the 497 252 participants [226 206 (45.5%) men, mean (SD) age, 57.5(8.1) years], 12 755 had ischaemic stroke, 6758 had a diagnosis of focal epilepsy, 3315 had Parkinson's disease, 2315 had multiple sclerosis, 559 had motor neurone disease and 18 254 had migraine either at study baseline or diagnosed during the follow-up period. Apart from motor neurone disease, all conditions had lower <i>pre-diagnosis</i> executive function compared to controls (assessment performed median 7.4 years before diagnosis). At a group level, focal epilepsy and multiple sclerosis showed a gradual worsening in executive function up to 15 years prior to diagnosis, while ischaemic stroke was characterised by a modest decline for a few years followed by a substantial reduction at the time of diagnosis. By contrast, participants with migraine showed a mild reduction in pre-diagnosis cognition compared to controls which improved following clinical diagnosis. Pre-diagnosis MRI GM volume was lower than controls for stroke, Parkinson's disease and multiple sclerosis (scans performed median 1.7 years before diagnosis), while other conditions had lower volumes post-diagnosis. These cognitive trajectory models reveal disease-specific temporal patterns at a group level, including a long cognitive prodrome associated with focal epilepsy and multiple sclerosis. The findings may help to prioritise risk management of individual diseases and inform clinical decision-making.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf307"},"PeriodicalIF":4.5,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12411756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnetomyographic evaluation of motor unit size that is robust to changes in distance to sensor.","authors":"Tai Otani, Miho Akaza, Shigenori Kawabata, Hirokazu Natsui, Taishi Watanabe, Yuki Miyano, Ryoichi Hanazawa, Yoshiaki Adachi, Kensuke Sekihara, Tadashi Kanouchi, Takanori Yokota","doi":"10.1093/braincomms/fcaf294","DOIUrl":"10.1093/braincomms/fcaf294","url":null,"abstract":"<p><p>In clinical practice, motor unit (MU) size is evaluated using needle electromyography to diagnose the cause of muscle weakness, whether myogenic or neurogenic. However, needle electromyography is influenced by the conductance of the muscle tissue and the distance from the MU to the electrode. In contrast, the magnetic field generated by a skeletal muscle is not distorted by subcutaneous tissues because their magnetic permeability is considered equal to that of free space. Therefore, we hypothesized that MU amplitude can be measured via magnetic field recordings. We tested this hypothesis by recording MU activity in the abductor pollicis brevis muscle. We then evaluated the MU size difference between healthy individuals and patients with spinal muscular atrophy and spinal-bulbar muscular atrophy. Furthermore, we assessed whether our method could consistently evaluate the MU size regardless of the sensor-muscle distance. Myomagnetic fields of single MUs evoked by electrical stimulation of the median nerve were measured. We used a biomagnetometer equipped with 132-channel superconducting quantum interference device sensors orientated upwards and arrayed on a quasi-planar surface. We applied a spatial filtering method that can estimate the current distribution from the magnetic field even for a conductor with unknown configuration or conductivity distribution and that does not require an a priori assumption of how many source currents are present. We visualized the electrical activity of 12 MUs of the abductor pollicis brevis muscle from eight healthy individuals and of two MUs from two patients with spinal muscular atrophy and spinal-bulbar muscular atrophy. Four current patterns were identified in the MU electrical activity. In all MUs, current towards the innervation zone was observed just after the start of activities. We called this current 'initial muscle-directing current'. At the same time, currents directed proximally and distally from the middle of the muscle were observed in most MUs. Initial muscle-directing current was more than 3 or 10 times larger in patients with spinal muscular atrophy and spinal-bulbar muscular atrophy than in healthy individuals. Initial muscle-directing current was estimated to weaken by 5.5% for every 5-mm increase in distance from the sensor array. Initial muscle-directing current is considered to reflect the activity near the neuromuscular junction and can be an index of MU size. The results confirmed our hypothesis that MU amplitude can be evaluated using magnetic measurements. This novel and non-invasive magnetomyography method can evaluate MU size with little influence of distance and has the potential to supersede needle electromyography.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 4","pages":"fcaf294"},"PeriodicalIF":4.5,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145133065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognitive and cerebral phenotypes of neurocognitive disorders due to alcohol or Alzheimer's disease.","authors":"Célia Soussi, Shailendra Segobin, Nicolas Cabé, Alice Laniepce, Laurent Coulbault, Céline Boudehent, Vincent de la Sayette, Gaël Chételat, Anne-Lise Pitel","doi":"10.1093/braincomms/fcaf289","DOIUrl":"10.1093/braincomms/fcaf289","url":null,"abstract":"<p><p>Distinguishing aetiologies of neurocognitive disorder (NCD) between alcohol-induced pathologies (OH) and Alzheimer's disease poses a major clinical challenge while dual diagnosis may be common. We aimed to define commonalities and specificities of neurocognitive alterations in OH or Alzheimer's Disease, considering the NCD severity (mild/major). In this retrospective cross-sectional study, we included 203 participants: 50 Mild-NCD-OH patients, 18 Major-NCD-OH patients, 30 Mild-NCD-AD patients, 24 Major-NCD-AD patients, as well as 81 healthy controls. Patients were compared on a neuropsychological and multimodal neuroimaging assessment (grey/white matter density and glucose metabolism). Analyses explored commonalities and specificities of each patient group within each NCD severity. All patient groups had episodic memory impairments, medial temporal lobe damage and hypometabolism in thalami and posteromedial cortex. NCD-AD patients had more severe cognitive deficits than NCD-OH patients, and the reverse pattern was observed for brain damage. NCD-OH patients notably showed more severe thalamic and cingulate alterations. NCD-OH patients also presented cerebellar damage not observed in NCD-AD. Volume deficits in the medial temporal lobe and memory deficits were more severe in Mild-NCD-AD than Mild-NCD-OH, but similar in Major-NCD-AD and Major-NCD-OH. Common alterations are observed in NCD-OH and NCD-AD, mainly within the memory circuit. Only cerebellar damage appears to be specific to NCD-OH. The specificity of NCD-AD deficits relies on their severity since they are also present to a lesser extent in NCD-OH, reinforcing how the neurocognitive phenotypes overlap. These results reaffirm the importance of questioning alcohol consumption in NCD-AD patients and considering an Alzheimer's Disease diagnosis in NCD-OH patients.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 4","pages":"fcaf289"},"PeriodicalIF":4.5,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12366719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}