Brain communications最新文献

{"title":"Correction to: The role of brain white matter in depression resilience and response to sleep interventions.","authors":"","doi":"10.1093/braincomms/fcaf064","DOIUrl":"https://doi.org/10.1093/braincomms/fcaf064","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/braincomms/fcad210.].</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf064"},"PeriodicalIF":4.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560388","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":"Longitudinal alterations in brain networks and thalamocortical connectivity in paediatric focal epilepsy: a structural connectomics pilot study.","authors":"Aswin Chari, Rory J Piper, Rachel Wilson-Jeffers, Michelle Ruiz-Perez, Kiran Seunarine, M Zubair Tahir, Chris A Clark, Richard Rosch, Rod C Scott, Torsten Baldeweg, Martin M Tisdall","doi":"10.1093/braincomms/fcaf081","DOIUrl":"10.1093/braincomms/fcaf081","url":null,"abstract":"<p><p>Epilepsy is an archetypal brain network disorder characterized by recurrent seizures and associated psychological, cognitive and behavioural sequelae. Progressive brain network dysfunction may contribute to poorer outcomes following treatment, but this has never been tested in humans. In this structural connectomics pilot study, we assess whether there is progressive brain network dysfunction in a cohort of 23 children undergoing repeated multi-shell diffusion tensor imaging as part of their pre-surgical evaluation of focal epilepsy prior to epilepsy surgery. We analyse global and nodal graph metrics and thalamocortical connectivity, comparing the longitudinal changes to a cross-sectional cohort of 57 healthy controls. We identify no robust longitudinal changes in global or nodal network properties over a median of 1.15 years between scans. We also do not identify robust longitudinal changes in thalamic connectivity between scans. On sensitivity analyses, we identify increases in weighted degree at higher scales of brain parcellation and a decrease in the proportion of nodes with a low participation coefficient, suggesting progressive increases in intermodular connections. These findings of no or subtle structural longitudinal brain network changes over a relatively short timeframe indicate that either there are no progressive structural brain network changes over time in epilepsy or the changes appear over longer timescales. Larger studies with longer timeframes between scans may help clarify these findings.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf081"},"PeriodicalIF":4.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560391","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":"Vulnerability of the entorhinal cortex II to neurodegeneration in Alzheimer's disease.","authors":"Aldelmo Emmanuel Reyes-Pablo, Nabil Itzi Luna-Viramontes, José Francisco Montiel-Sosa, Miguel Ángel Ontiveros-Torres, Linda Garcés-Ramírez, Fidel de la Cruz-López, Ricardo Apátiga-Pérez, Ignacio Villanueva-Fierro, Mario Hernandes-Alejandro, Blanca Estela Jaramillo-Loranca, Genaro Vargas-Hernández, Mar Pacheco-Herrero, José Luna-Muñoz","doi":"10.1093/braincomms/fcaf091","DOIUrl":"10.1093/braincomms/fcaf091","url":null,"abstract":"<p><p>Alzheimer's disease is characterized by progressive memory loss and deterioration of cognitive functions. The presence of neurofibrillary tangles in the hippocampal areas (perforant pathway) correlates with cognitive impairment. Pathological processing of tau protein is characterized by post-translational changes such as hyperphosphorylation and truncation, which favour conformational changes within tau. These conformational changes can be regional (dependent on phosphorylation) or structural (depending on regional conformational changes and truncation). Through immunohistochemical and immunofluorescence staining in hippocampus Alzheimer disease brains and quantification in tissue stained with TG3 antibody and analysed by confocal microscopy, we have been able to demonstrate that TG3 correlates with cognitive impairment. In the process of tangle evolution, TG3 is present in pre-tangle. This epitope of the TG3 antibody was very stable to proteolytic processing by caspase-3; truncation is evidenced by the TauC-3 antibody. The entorhinal cortex showed high sensitivity to neurodegeneration and pathological tau processing.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf091"},"PeriodicalIF":4.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143618057","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":"Neural correlates of fatigue after traumatic brain injury.","authors":"Annina E Anliker, Léa A S Chauvigné, Leslie Allaman, Adrian G Guggisberg","doi":"10.1093/braincomms/fcaf082","DOIUrl":"10.1093/braincomms/fcaf082","url":null,"abstract":"<p><p>Fatigue is the main cause of disability after traumatic brain injury and has negative impact on social, physical and cognitive functions, participation in daily activities, and ability to work. Since the neural underpinnings are largely unknown, few causal treatments are currently available. This study therefore aimed to investigate the neural correlates of subjective fatigue after traumatic brain injury, controlling for differences in cognitive performance, motor performance and subjective psychological covariates such as depression, anxiety and apathy. Seventeen chronic traumatic brain injury patients (10 with and seven without fatigue) and 11 age, sex, and education-matched healthy controls participated in the study. The dependent variable, overall fatigue, was quantified as the sum of the subscales of the multivariate fatigue inventory. Subjective psychological covariates were extracted from appropriate questionnaires. Brain activation during a two-back task and functional connectivity at rest were reconstructed from high-density EEG. Cortical excitability was quantified from motor evoked potentials induced by transcranial magnetic stimulation over the primary motor cortex. Cognitive performance was assessed with a two-back task as well as with a comprehensive neuropsychological test battery. Motor performance was quantified with Jamar dynamometer. Beside the between-group differences in most fatigue subscales resulting from the group attribution, participants also differed in subjective memory functions, depression, anxiety and apathy. Conversely, objective neuropsychological performance was similar across groups in most domains, except for alertness and divided attention (<i>P</i> ≤ 0.039). At the neural level, we observed no difference in corticospinal excitability, but a significant disruption of global resting-state alpha-band functional connectivity between cortical midline structures and the rest of the brain in patients with fatigue (<i>P</i> = 0.006). Furthermore, individuals with fatigue exhibited reduced signs of overall brain activation compared with healthy controls throughout the cognitive task (<i>P</i> = 0.032) without time-on-task effect. In a multivariate regression model, resting-state functional connectivity (<i>P</i> = 0.013) and subjective psychological questionnaire scores (<i>P</i> < 0.0001) were independent predictors of fatigue. In conclusion, our results suggest that disrupted network interactions are the primary independent neural predictor of fatigue. This may serve as a new target for therapy.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf082"},"PeriodicalIF":4.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598601","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":"Plasma biomarkers for diagnosis and differentiation and their cognitive correlations in patients with Alzheimer's disease.","authors":"Wenhao Sun, Shuwei Ye, Yu Wang, Huifeng Chen, Ping Che, Jingshan Chen, Nan Zhang","doi":"10.1093/braincomms/fcaf094","DOIUrl":"10.1093/braincomms/fcaf094","url":null,"abstract":"<p><p>Increasing evidence has shown the potential value of plasma biomarkers in Alzheimer's disease diagnosis. This study aimed to determine the diagnostic and differential values of emerging plasma biomarkers for different types of dementia in a Chinese population and to explore their cognitive correlations. One hundred twenty patients with dementia, including 51 Alzheimer's disease patients, 54 subcortical ischaemic vascular dementia (SIVD) patients and 15 frontotemporal lobar degeneration (FTLD) patients were recruited alongside 27 cognitively unimpaired (CU) control subjects. Global and domain-specific cognition was assessed in all participants by a battery of neuropsychological tests. Plasma amyloid-beta (Αβ)42, Aβ40 and total tau (in CU controls and Alzheimer's disease patients) and phosphorylated tau at threonine-181 (<i>P</i>-tau181), neurofilament light (NfL) and glial fibrillar acidic protein (GFAP) levels (in all participants) were measured using the single-molecule array platform. The levels of all biomarkers differed between Alzheimer's disease patients and CU controls, with <i>P</i>-tau181 and GFAP levels and the Aβ42/P-tau181 ratio best differentiating the two groups [area under the curve (AUC) = 0.966, 0.932 and 0.927, respectively]. P-tau181 and GFAP levels were greater in the Alzheimer's disease group than in the other two patient groups and showed the best performance in distinguishing Alzheimer's disease patients from SIVD (AUC = 0.922) and FTLD patients (AUC = 0.894), respectively. Moreover, compared with that in the CU group, the GFAP level was elevated in the SIVD group, and the NfL level was elevated in all patient groups. Compared with other single biomarkers, the plasma Aβ42/P-tau181 ratio correlated with broader cognitive domains, including global cognition [Mini-Mental Status Examination (MMSE), <i>r</i> = 0.314, <i>P</i> = 0.027; Montreal Cognitive Assessment (MoCA), <i>r</i> = 0.313, <i>P</i> = 0.043], memory (<i>r</i> = 0.339, <i>P</i> = 0.016), language (<i>r</i> = 0.333, <i>P</i> = 0.020), attention and information processing speed (<i>r</i> = 0.369, <i>P</i> = 0.008), executive function (<i>r</i> = 0.305, <i>P</i> = 0.031) and visuospatial function memory (<i>r</i> = 0.453, <i>P</i> = 0.001). P-tau181 was an optimal plasma biomarker for identifying Alzheimer's disease patients and differentiating Alzheimer's disease patients from SIVD and FTLD patients. Moreover, the GFAP level and the Aβ42/P-tau181 ratio showed potential diagnostic and progression monitoring value, respectively, for Alzheimer's disease patients.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf094"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569124","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":"Could immunotherapy and regulatory T cells be used therapeutically to slow the progression of Alzheimer's disease?","authors":"Victoria Abbott, Benjamin E Housden, Annwyne Houldsworth","doi":"10.1093/braincomms/fcaf092","DOIUrl":"10.1093/braincomms/fcaf092","url":null,"abstract":"<p><p>Alzheimer's disease and other cognitive impairments are a growing problem in the healthcare world with the ageing population. There are currently no effective treatments available; however, it has been suggested that targeting neuroinflammation may be a successful approach in slowing the progression of neurodegeneration. Reducing the destructive hyperinflammatory pathology to maintain homeostasis in neural tissue is a promising option to consider. This review explores the mechanisms behind neuroinflammation and the effectiveness of immunotherapy in slowing the progression of cognitive decline in patients with Alzheimer's disease. The key components of neuroinflammation in Alzheimer's disease researched are microglia, astrocytes, cytokines and CD8+ effector T cells. The role of oxidative stress on modulating regulatory T cells and some of the limitations of regulatory T cell-based therapies are also explored. Increasing regulatory T cells can decrease activation of microglia, proinflammatory cytokines and astrocytes; however, it can also increase levels of inflammatory cytokines. There is a complex network of regulatory T cell interactions that reduce Alzheimer's disease pathology, which is not fully understood. Exploring the current literature, further research into the use of immunotherapy in Alzheimer's disease is vital to determine the potential of these techniques; however, there is sufficient evidence to suggest that increasing regulatory T cells count does prevent Alzheimer's disease symptoms and pathology in patients with Alzheimer's disease. Some exciting innovative therapies are muted to explore in the future. The function of regulatory T cells in the presence of reactive oxygen species and oxidative stress should be investigated further in patients with neurogenerative disorders to ascertain if combination therapies could reduce oxidative stress while also enhancing regulatory T cells function. Could methods of immunotherapy infuse exogenous functional Tregs or enhance the immune environment in favour of endogenous regulatory T cells differentiation, thus reducing neuroinflammation in neurodegenerative pathology, inhibiting the progression of Alzheimer's disease?</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf092"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11896979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143618056","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":"The role of microglia in the prion-like transmission of protein aggregates in neurodegeneration.","authors":"Muhammet M Öztürk, Jakob Emgård, Juan García-Revilla, Rosalía Fernández-Calle, Yiyi Yang, Tomas Deierborg, Tomas T Roos","doi":"10.1093/braincomms/fcaf087","DOIUrl":"10.1093/braincomms/fcaf087","url":null,"abstract":"<p><p>Numerous neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis share a neuropathological hallmark: aberrant protein aggregation in the CNS. Microglia, the brain's innate immune cells, also play a pivotal role in the pathogenesis of these disorders. Multiple studies indicate that these pathological aggregates can propagate throughout the brain in a prion-like manner. A protein/peptide that adopts a prion-like conformation can induce homologous proteins to misfold into a prion-like conformation through templated seeding, enabling cell-to-cell spread and accelerating protein aggregation throughout the brain. Two important questions in the prion-like paradigm are where the prion-like misfolding occurs and how the prion-like aggregates are spread throughout the CNS. Here, we review the role of microglia and associated inflammation in the prion-like spread of pathologically aggregated proteins/peptides in Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. A growing body of evidence suggests that microglia can internalize prion-like proteins and transport them to neighbouring neurons and other glial cells. Microglia may also influence the potential seeding of proteins in neurons and induce inflammatory pathways in their microenvironment. This review aims to broaden the understanding of the role of microglia in the prion-like spread of protein aggregation.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf087"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569177","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":"Anti-seizure medication tapering correlates with daytime delta band power reduction in the cortex.","authors":"Guillermo M Besné, Nathan Evans, Mariella Panagiotopoulou, Billy Smith, Fahmida A Chowdhury, Beate Diehl, John S Duncan, Andrew W McEvoy, Anna Miserocchi, Jane de Tisi, Matthew C Walker, Peter N Taylor, Chris Thornton, Yujiang Wang","doi":"10.1093/braincomms/fcaf020","DOIUrl":"10.1093/braincomms/fcaf020","url":null,"abstract":"<p><p>Anti-seizure medications are the primary treatment for epilepsy; yet medication tapering effects have not been investigated in a dose, region and time-dependent manner, despite their potential impact on research and clinical practice. We examined over 3000 h of intracranial EEG recordings in 32 subjects during long-term monitoring, of which 22 underwent concurrent anti-seizure medication tapering. We estimated anti-seizure medication plasma levels based on known pharmaco-kinetics of all the major anti-seizure medication types. We found an overall decrease in the power of delta band (<i>δ</i>) activity around the period of maximum medication withdrawal in most (80%) subjects, independent of their epilepsy type or medication combination. The degree of withdrawal correlated positively with the magnitude of <i>δ</i> power decrease. This dose-dependent effect was evident across all recorded cortical regions during daytime; but not in subcortical regions, or during night time. We found no evidence of a differential effect in seizure onset, spiking, or pathological brain regions. The finding of decreased <i>δ</i> band power during anti-seizure medication tapering agrees with previous literature. Our observed dose-dependent effect indicates that monitoring anti-seizure medication levels in cortical regions may be feasible for applications such as medication reminder systems, or closed-loop anti-seizure medication delivery systems. Anti-seizure medications are also used in other neurological and psychiatric conditions, making our findings relevant to a general neuroscience and neurology audience.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf020"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506057","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":"'Hyperbinding' in functional movement disorders: role of supplementary motor area efferent signalling.","authors":"Anirban Dutta","doi":"10.1093/braincomms/fcae464","DOIUrl":"10.1093/braincomms/fcae464","url":null,"abstract":"","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae464"},"PeriodicalIF":4.1,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11848267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495029","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":"Response to: 'Hyperbinding' in functional movement disorders: role of supplementary motor area efferent signalling.","authors":"Bernhard Pastötter, Anne Weissbach, Adam Takacs, Josephine Moyé, Julius Verrel, Fabian Chwolka, Julia Friedrich, Theresa Paulus, Simone Zittel, Tobias Bäumer, Christian Frings, Christian Beste, Alexander Münchau","doi":"10.1093/braincomms/fcae465","DOIUrl":"10.1093/braincomms/fcae465","url":null,"abstract":"","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae465"},"PeriodicalIF":4.1,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11848266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495033","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}