Brain communications最新文献

{"title":"Diagnosis of cognitive impairment and dementia: blood plasma and optical coherence tomography.","authors":"Vidishaa Jali, Qinglin Zhang, Joyce Ruifen Chong, Damon Wong, Bingyao Tan, Gerhard Garhöfer, Saima Hilal, Mitchell K P Lai, Leopold Schmetterer, Christopher Li-Hsian Chen, Jacqueline Chua","doi":"10.1093/braincomms/fcae472","DOIUrl":"10.1093/braincomms/fcae472","url":null,"abstract":"<p><p>Accurate and early diagnosis of Alzheimer's disease and vascular dementia is crucial for enabling timely interventions and improving patient outcomes. This study evaluates the diagnostic performance of plasma biomarkers (neurofilament light chain and phosphorylated tau181) and retinal biomarkers (retinal nerve fibre layer and ganglion cell-inner plexiform layer), individually and in combination, in differentiating moderate cognitive impairment and dementia from mild cognitive impairment and no cognitive impairment. A cross-sectional study was conducted involving 509 participants, aged 50 and older, recruited from a memory clinic. The participants were categorized as normal (<i>n</i> = 100), mild cognitive impairment (<i>n</i> = 144), moderate cognitive impairment (<i>n</i> = 90) or dementia (<i>n</i> = 175) based on detailed clinical assessments, neuropsychological testing and MRI scans. The thickness of the ganglion cell-inner plexiform layer (<i>P</i> < 0.001) and retinal nerve fibre layer (<i>P</i> = 0.030) decreased progressively from normal cognition to cognitive impairment and dementia. The thickest layers were observed in individuals with no cognitive impairment (mean ± standard deviation: ganglion cell-inner plexiform layer: 76 ± 11 µm, retinal nerve fibre layer: 92 ± 10 µm), while the thinnest layers were found in individuals with dementia (ganglion cell-inner plexiform layer: 72 ± 14 µm, retinal nerve fibre layer: 89 ± 12 µm). Plasma biomarker levels increased progressively from normal cognition to cognitive impairment and dementia (<i>P</i> < 0.001). Levels were lowest in individuals with no cognitive impairment [median (interquartile range): neurofilament light chain: 15 (9) pg/mL, phosphorylated tau181: 1.85 (1.00) pg/mL] and highest in those with dementia [neurofilament light chain: 34 (27) pg/mL, phosphorylated tau181: 3.24 (2.81) pg/mL]. After adjusting for retinal scan signal strength, neurofilament light chain showed a stronger negative association with retinal nerve fibre layer thickness [standardized beta estimate (<i>β</i>) = -0.184] and ganglion cell-inner plexiform layer thickness (<i>β</i> = -0.139) compared to phosphorylated tau181, which exhibited weaker associations with ganglion cell-inner plexiform layer (<i>β</i> = -0.091) and retinal nerve fibre layer (<i>β</i> = -0.059). While retinal parameters provided modest discriminatory ability (AUC = 0.60), plasma biomarkers demonstrated superior diagnostic performance (AUC = 0.76). Notably, neurofilament light chain had a stronger association with retinal thinning than phosphorylated tau181 and offered superior diagnostic value for identifying moderate cognitive decline. These findings underscore the potential of plasma biomarkers, particularly neurofilament light chain, for the early detection of dementia.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae472"},"PeriodicalIF":4.1,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142924200","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":"A 50-year data-driven model of disability and lesion load trajectories in progressive multiple sclerosis.","authors":"Neil P Oxtoby, Frederik Barkhof","doi":"10.1093/braincomms/fcae474","DOIUrl":"https://doi.org/10.1093/braincomms/fcae474","url":null,"abstract":"<p><p>This scientific commentary refers to 'A data-driven model of disability progression in progressive multiple sclerosis', by Garbarino <i>et al</i>. (https://doi.org/10.1093/braincomms/fcae434).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae474"},"PeriodicalIF":4.1,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11704779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960232","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":"Advances in assessment and cognitive neurorehabilitation of HIV-related neurocognitive impairment.","authors":"Elia L Fischer, Alexis Renaud, Petr Grivaz, Giovanni Di Liberto, Philippe Ryvlin, Matthias Cavassini, Renaud A Du Pasquier, Arseny A Sokolov","doi":"10.1093/braincomms/fcae399","DOIUrl":"10.1093/braincomms/fcae399","url":null,"abstract":"<p><p>Neurocognitive impairment (NCI) is present in around 40% of people with HIV and substantially affects everyday life, adherence to combined antiretroviral therapy (cART) and overall life expectancy. Suboptimal therapy regimen, opportunistic infections, substance abuse and highly prevalent psychiatric co-morbidities contribute to NCI in people with HIV. In this review, we highlight the need for efficacious treatment of HIV-related NCI through pharmacological approaches and cognitive neurorehabilitation, discussing recent randomized controlled trials in this domain. We also discuss the benefits of a thorough and interdisciplinary diagnostic work-up between specialists in neurology, psychiatry, neuropsychology and infectious diseases, helping to disentangle the various factors contributing to cognitive complaints and deficits in people with HIV. While the advent of cART has contributed to slowing the progression of cognitive deficits in people with HIV and reducing the prevalence of HIV-associated dementia, NCI persists at a significant rate. Adjuvant stimulating or neuroprotective pharmacological agents have shown some potential benefits. Despite promising outcomes, studies on cognitive neurorehabilitation of HIV-related NCI remain sparse and limited in terms of methodological aspects. The access to cognitive neurorehabilitation is also restricted, in particular at the global scale. Novel technology bears a significant potential for restoring cognitive function in people with HIV, affording high degrees of standardization and personalization, along with opportunities for telerehabilitation. Entertaining serious video game environments with immersive graphics can further promote patient motivation, training adherence and impact on everyday life, as indicated by a growing body of evidence, including in seropositive children and older individuals in Africa. Upon validation of technology-assisted cognitive neurorehabilitation for HIV-related NCI in large-scale randomized controlled trials with state-of-the-art methodology, these approaches will promote socio-professional reintegration and quality of life of people with HIV.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae399"},"PeriodicalIF":4.1,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11670355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901217","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":"Data management (and sharing) in neuroscience: balancing possible, practical and perfect solutions.","authors":"Tara L Spires-Jones","doi":"10.1093/braincomms/fcae450","DOIUrl":"10.1093/braincomms/fcae450","url":null,"abstract":"<p><p>Our editor discusses re-organizing her lab's data storage to facilitate sharing and archiving data. She also advertises the 'Brain Communications' early career researcher paper prize for the first author of a paper published in the journal in 2024-please send nominations!</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae450"},"PeriodicalIF":4.1,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901221","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":"Predicting incident dementia in community-dwelling older adults using primary and secondary care data from electronic health records.","authors":"Konstantin Georgiev, Yiqing Wang, Andrew Conkie, Annie Sinclair, Vyron Christodoulou, Saleh Seyedzadeh, Malcolm Price, Ann Wales, Nicholas L Mills, Susan D Shenkin, Joanne McPeake, Jacques D Fleuriot, Atul Anand","doi":"10.1093/braincomms/fcae469","DOIUrl":"https://doi.org/10.1093/braincomms/fcae469","url":null,"abstract":"<p><p>Predicting risk of future dementia is essential for primary prevention strategies, particularly in the era of novel immunotherapies. However, few studies have developed population-level prediction models using existing routine healthcare data. In this longitudinal retrospective cohort study, we predicted incident dementia using primary and secondary care health records at 5, 10 and 13 years in 144 113 Scottish older adults who were dementia-free prior to 1st April 2009. Gradient-boosting (XGBoost) prediction models were trained on two feature subsets: data-driven (using all 171 extracted variables) and clinically supervised (22 curated variables). We used a random-stratified internal validation set to rank top predictors in each model, assessing performance stratified by age and socioeconomic deprivation. Predictions were stratified into 10 equally sized risk deciles and ranked by response rate. Over 13 years of follow-up, 11 143 (8%) patients developed dementia. The data-driven models achieved marginally better precision-recall area-under-the-curve scores of 0.18, 0.26 and 0.30 compared to clinically supervised models with scores of 0.17, 0.27 and 0.29 for incident dementia at 5, 10 and 13 years, respectively. The clinically supervised model achieved comparable specificity 0.88 [95% confidence interval (CI) 0.87-0.88] and sensitivity (0.55, 95% CI 0.53-0.57) to the data-driven model for prediction at 13 years. The most important model features were age, deprivation and frailty, measured by a modified electronic frailty index excluding known cognitive deficits. Model precision was consistent across socioeconomic deprivation quintiles but lower in younger-onset (<70 years) dementia cases. At 13 years, dementia was diagnosed in 32% of the population classified as highest risk with 40% of individuals in this group below the age of 80. Personalized estimates of future dementia risk from routinely collected healthcare data could influence risk factor modification and help to target brain imaging and novel immunotherapies in selected individuals with pre-symptomatic disease.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae469"},"PeriodicalIF":4.1,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933961","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":"Complex I deficiency remains the most frequent cause of Leigh syndrome spectrum.","authors":"Shamima Rahman","doi":"10.1093/braincomms/fcae470","DOIUrl":"https://doi.org/10.1093/braincomms/fcae470","url":null,"abstract":"<p><p>This scientific commentary refers to 'Biallelic <i>NDUFA13</i> variants lead to a neurodevelopmental phenotype with gradual neurological impairment', by Kaiyrzhanov <i>et al</i>. (https://doi.org/10.1093/braincomms/fcae453).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae470"},"PeriodicalIF":4.1,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018054","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":"Impaired semantic control in the logopenic variant of primary progressive aphasia.","authors":"Shalom K Henderson, Siddharth Ramanan, Matthew A Rouse, Thomas E Cope, Ajay D Halai, Karalyn E Patterson, James B Rowe, Matthew A Lambon Ralph","doi":"10.1093/braincomms/fcae463","DOIUrl":"10.1093/braincomms/fcae463","url":null,"abstract":"&lt;p&gt;&lt;p&gt;We investigated semantic cognition in the logopenic variant of primary progressive aphasia, including (i) the status of verbal and non-verbal semantic performance; and (ii) whether the semantic deficit reflects impaired semantic control. Our &lt;i&gt;a priori&lt;/i&gt; hypothesis that individuals with logopenic variant of primary progressive aphasia would exhibit semantic control impairments was motivated by the anatomical overlap between the temporoparietal atrophy typically associated with logopenic variant of primary progressive aphasia and lesions associated with post-stroke semantic aphasia and Wernicke's aphasia, which cause heteromodal semantic control impairments. We addressed the presence, type (semantic representation and semantic control; verbal and non-verbal), and progression of semantic deficits in logopenic variant of primary progressive aphasia. Since most people with logopenic variant of primary progressive aphasia have Alzheimer's disease pathology and are part of a broader multi-dimensional phenotype space encompassing Alzheimer's disease sub-types, we compared semantic performance in logopenic variant of primary progressive aphasia and typical amnestic Alzheimer's disease. Given the differences in lesion and atrophy patterns in semantic aphasia and Wernicke's aphasia versus semantic-dementia/semantic-variant primary progressive aphasia patients, our second aim was to examine atrophy patterns in people with logopenic variant of primary progressive aphasia and typical Alzheimer's disease compared to age-matched controls. Twenty-seven patients participated in the study. People were grouped into those meeting consensus criteria for logopenic variant of primary progressive aphasia (&lt;i&gt;N&lt;/i&gt; = 10) and others who may have previously satisfied definitions of logopenic variant of primary progressive aphasia but had progressed with multi-domain cognitive impairments (herein referred to as 'logopenic variant of primary progressive aphasia+'; &lt;i&gt;N&lt;/i&gt; = 8). People with typical amnestic Alzheimer's disease (&lt;i&gt;N&lt;/i&gt; = 9) were relatively preserved across verbal and non-verbal semantic assessments. Logopenic variant of primary progressive aphasia patients were impaired on both verbal and non-verbal semantic tasks and their impairments showed the hallmark characteristics of a semantic control deficit. Logopenic variant of primary progressive aphasia and logopenic variant of primary progressive aphasia + patients showed effects of varying semantic control demands, positive cueing effects, and correlated performance between semantic and executive tasks. Whole-brain voxel-based morphometry, comparing each of the patient groups to age-matched controls, revealed significantly reduced grey and white matter in the bilateral hippocampi and lateral temporal regions in typical Alzheimer's disease patients. The logopenic variant of primary progressive aphasia group exhibited an asymmetric pattern of reduced grey and white matter intensity in the language-domi","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae463"},"PeriodicalIF":4.1,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973620","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":"Complex auditory regularity processing across levels of consciousness in coma: Stage 1 Registered Report.","authors":"Andria Pelentritou, Jacinthe Cataldi, Frederic Zubler, Manuela Iten, Matthias Haenggi, Nawfel Ben-Hamouda, Andrea O Rossetti, Athina Tzovara, Marzia De Lucia","doi":"10.1093/braincomms/fcae466","DOIUrl":"10.1093/braincomms/fcae466","url":null,"abstract":"<p><p>A key question for the scientific study of consciousness is whether it is possible to identify specific features in brain activity that are uniquely linked to conscious experience. This question has important implications for the development of markers to detect covert consciousness in unresponsive patients. In this regard, many studies have focused on investigating the neural response to complex auditory regularities. One noteworthy example is the local global paradigm, which allows for the investigation of auditory regularity encoding at the 'global' level, based on the repetition of groups of sounds. The inference of global regularities is thought to depend on conscious access to such complex auditory stimuli as mostly shown in chronic stages of disorders of consciousness patients. However, whether global regularity encoding can identify covert consciousness along the consciousness spectrum including earlier stages of these disorders remains controversial. Here, we aim to fill this gap by investigating whether the inference of global auditory regularities can occur in acute coma, in the absence of consciousness, and how this may be modulated by the severity of the patients' clinical condition and consciousness level measured using the Full Outline of UnResponsiveness (FOUR) score. We will acquire 63-channel continuous electroencephalography to measure the neural response to global auditory regularity in comatose patients (<i>N</i> = 30) during the first day after cardiac arrest, when patients are unconscious, sedated and under normothermia, and during the second day (with reduced or absent sedation and body temperature control). We hypothesize that global regularity encoding will persist in the absence of consciousness independent of patient outcome, observed as above chance decoding of the neural response to global regularities using multivariate decoding analyses. We further hypothesize that decoding performance will positively correlate with the FOUR score, which indexes consciousness level, and typically improves between the first and second day after coma onset following cardiac arrest in patients with favourable outcome. In an exploratory analysis, we will also evaluate whether global regularity encoding may be influenced by the patients' clinical management, specifically sedation, also shown to affect global deviance detection. Our results will shed light on the neurophysiological correlates of complex auditory regularity processing in unconscious patients and on the link to residual levels of consciousness during the underexplored state of coma upon the first days after cardiac arrest.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae466"},"PeriodicalIF":4.1,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11735756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017910","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":"Brain age in genetic and idiopathic Parkinson's disease.","authors":"Stefan J Teipel, Hauke Hoffmann, Alexander Storch, Andreas Hermann, Martin Dyrba, Julia Schumacher","doi":"10.1093/braincomms/fcae382","DOIUrl":"10.1093/braincomms/fcae382","url":null,"abstract":"<p><p>The brain-age gap, i.e. the difference between the brain age estimated from structural MRI data and the chronological age of an individual, has been proposed as a summary measure of brain integrity in neurodegenerative diseases. Here, we aimed to determine the brain-age gap in genetic and idiopathic Parkinson's disease and its association with surrogate markers of Alzheimer's disease and Parkinson's disease pathology and with rates of cognitive and motor function decline. We studied 1200 cases from the Parkinson's Progression Markers Initiative cohort, including idiopathic Parkinson's disease, asymptomatic and clinical mutation carriers in the leucine-rich repeat kinase 2 gene (LRRK2) and the glucocerebrosidase gene (GBA), and normal controls using a cohort study design. For comparison, we studied 187 Alzheimer's disease dementia cases and 254 controls from the Alzheimer's Disease Neuroimaging Initiative cohort. We used Bayesian ANOVA to determine associations of the brain-age gap with diagnosis, and baseline measures of motor and cognitive function, dopamine transporter activity and CSF markers of Alzheimer's disease type amyloid-β42 and phosphotau pathology. Associations of brain-age gap with rates of cognitive and motor function decline were determined using Bayesian generalized mixed effect models. The brain-age gap in idiopathic Parkinson's disease patients was 0.7 years compared to controls, but 5.9 years in Alzheimer's disease dementia cases. In contrast, asymptomatic LRRK2 individuals had a 1.1. year younger brain age than controls. Across all cases, the brain-age gap was associated with motor impairment and (in the clinically manifest PD cases) reduced dopamine transporter activity, but less with CSF amyloid-β42 and phosphotau. In idiopathic Parkinson's disease cases, however, the brain-age gap was associated with lower CSF amyloid-β42 levels. In sporadic and genetic Parkinson's disease cases, a higher brain-age gap was associated with faster decline in episodic memory, and executive and motor function, whereas in asymptomatic LRRK2 cases, a smaller brain-age gap was associated with faster cognitive decline. In conclusion, brain age was sensitive to Alzheimer's disease like rather than Parkinson's disease like brain atrophy. Once an individual had idiopathic Parkinson's disease, their brain age was associated with markers of Alzheimer's disease rather than Parkinson's disease. Asymptomatic LRRK2 cases had seemingly younger brains than controls, and in these cases, younger brain age was associated with poorer cognitive outcome. This suggests that the term brain age is misleading when applied to disease stages where reactive brain changes with apparent volume increases rather than atrophy may drive the calculation of the brain age.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 6","pages":"fcae382"},"PeriodicalIF":4.1,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11660940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878959","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":"Preserved social facilitation and preferential processing of partner-relevant information in Huntington's disease.","authors":"Jan Van den Stock, Gert Cypers, François-Laurent De Winter, Mathieu Vandenbulcke","doi":"10.1093/braincomms/fcae462","DOIUrl":"10.1093/braincomms/fcae462","url":null,"abstract":"<p><p>This scientific commentary refers to 'The joint memory effect: challenging the selfish stigma in Huntington's disease?', by Dalléry <i>et al</i>. (https://doi.org/10.1093/braincomms/fcae440).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae462"},"PeriodicalIF":4.1,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142916572","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}