Brain communications最新文献

{"title":"Altered static and dynamic functional connectivity in childhood basic-type intermittent exotropia.","authors":"Mengdi Zhou, Qinglei Shi, Huixin Li, Mengqi Su, Haoran Zhang, Jie Hong, Xiwen Wang, Xiang Wan, Jing Fu, Zhaohui Liu","doi":"10.1093/braincomms/fcaf358","DOIUrl":"10.1093/braincomms/fcaf358","url":null,"abstract":"<p><p>This study aimed to investigate static and dynamic functional connectivity alterations between the primary visual cortex, secondary visual cortex, higher visual cortex and oculomotor cortex in children with basic-type intermittent exotropia. A total of 44 children with basic-type intermittent exotropia and 37 healthy controls matched for sex, age and education level were included and underwent resting-state functional MRI. Both sides of Brodmann area (BA) 17, BA18, BA19 and BA8 were chosen as regions of interest. Sliding window method and <i>k</i>-means clustering analysis were employed to investigate static and dynamic functional connectivity as well as temporal metrics based on visual cortices and oculomotor cortices. Differences in functional connectivity and temporal metrics were identified and subsequently correlated with clinical characteristics using Pearson correlation analysis. Diagnostic efficacy of static and dynamic functional connectivity as well as near stereoacuity was assessed using receiver operating characteristic analysis. For static functional connectivity analysis, compared with healthy controls, children with intermittent exotropia showed decreased static functional connectivity between the right higher visual cortex (BA19) and the left oculomotor cortex (BA8), as well as between bilateral oculomotor cortices (BA8). For dynamic functional connectivity analysis, children with intermittent exotropia showed increased dynamic functional connectivity variability between the right secondary visual cortex (BA18) and the left higher visual cortex (BA19), as well as between the left higher visual cortex (BA19) and the right oculomotor cortex (BA8). In addition, the mean dwell time and fraction time in a specific state characterized by negative connectivity between visual cortices and oculomotor cortices were positively correlated with the disease duration. Receiver operating characteristic analyses demonstrated that the combination of static and dynamic functional connectivity exhibited high diagnostic performance for basic-type intermittent exotropia. Children with basic-type intermittent exotropia exhibited aberrant static and dynamic functional connectivity within the bilateral visual-oculomotor cortex pathways, which might be associated with visual perception and eye movement impairments. With the prolongation of disease duration, more time spent in a specific state might be related to aggravated eye movement disorder. The combination of static and dynamic functional connectivity provides a new perspective for exploring the neuropathological mechanisms of basic-type intermittent exotropia and offers a potential neuroimaging biomarker for diagnosis.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf358"},"PeriodicalIF":4.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12485606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214692","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":"Hyperpolarized [1-¹³C]pyruvate magnetic resonance spectroscopic imaging identifies elevated lactate in epileptic tissue.","authors":"Aditya Jhajharia, Mitchell Moyer, Jemima Olu-Owotade, Darrian McAfee, Abubakr Eldirdiri, Joshua Rogers, Minjie Zhu, Ujwal Boddeti, Riccardo Serra, J Marc Simard, Volodymyr Gerzanich, Muznabanu Bachani, Dirk Mayer, Alexander Ksendzovsky","doi":"10.1093/braincomms/fcaf357","DOIUrl":"10.1093/braincomms/fcaf357","url":null,"abstract":"<p><p>Thirty percent of epilepsy patients have seizures despite best medical therapy. While epilepsy surgery has emerged as a promising treatment option for these patients, surgical outcomes vary considerably between patients and have not significantly improved over the years. These stagnant outcomes can be attributed to poor seizure onset zone and epileptic network localization with currently available tools. Lactate production is a well-known consequence of metabolic reprogramming and biomarker in epilepsy. Detection of lactate elevations using conventional magnetic resonance spectroscopy has been extensively studied as an effective tool to non-invasively detect epileptic brain tissue. However, this method suffers from poor spatial resolution, which limits its clinical utility in presurgical resection mapping. In this study, we explore the utility of a recently developed approach, magnetic resonance spectroscopy and spectroscopic imaging of hyperpolarized [1-¹³C]pyruvate, to identify epileptic tissues via detection of increased lactate production. We found that this approach accurately identifies elevated lactate production in an <i>in vitro</i> model of chronic hyperactivity and in the gold standard mouse epilepsy model, pentylenetetrazol kindling. These data suggest that magnetic resonance spectroscopic imaging of hyperpolarized [1-¹³C]pyruvate has the potential to effectively and non-invasively map epileptic foci and should be further explored as a clinical tool to guide epilepsy resection surgery by identifying epileptic tissue in patients.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf357"},"PeriodicalIF":4.5,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12464677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187973","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":"Effects of Parkinson's disease on survival in cancer survivors: a retrospective, multicentre cohort study in Japan.","authors":"Kanako Asai, Yasufumi Gon, Yasuyoshi Kimura, Toshitaka Morishima, Hideki Mochizuki, Isao Miyashiro","doi":"10.1093/braincomms/fcaf347","DOIUrl":"10.1093/braincomms/fcaf347","url":null,"abstract":"<p><p>Aging populations and advances in medical care have contributed to an increase in the number of patients with Parkinson's disease and cancer survivors. However, the effects of Parkinson's disease on the survival of patients with cancer remain unclear. We aimed to investigate the effect of Parkinson's disease on the prognosis of patients with cancer. This retrospective multicentre cohort study used data from the Osaka Cancer Registry, which was linked to administrative data obtained between 2010 and 2015 in Japan. Patients with cancer who were followed up for 5 years after cancer diagnosis were categorized into Parkinson's disease and non- Parkinson's disease groups according to the presence of comorbid Parkinson's disease. We compared survival between the two groups using Kaplan-Meier analyses. Cox proportional-hazard models were used to assess the hazard ratio and 95% confidence interval of Parkinson's disease for all-cause mortality. Propensity-score matching was used to validate the analysis and address differences in clinical characteristics between the groups. The cohort included 118 999 patients with cancer and 1049 patients (0.9%) with comorbid Parkinson's disease. The patients in the Parkinson's disease group were older and had lower mobility than those in the non- Parkinson's disease group. Kaplan-Meier analysis revealed that the 5-year survival rate after cancer diagnosis was significantly worse in the Parkinson's disease group than in the non- Parkinson's disease group (54% versus 70%, <i>P</i> < 0.001). Comorbid Parkinson's disease was independently associated with 5-year mortality [crude hazard ratio (95% confidence interval), 1.72 (1.56-1.88), <i>P</i> < 0.001]. This association remained significant after adjusting for potential confounders [adjusted hazard ratio (95% confidence interval), 1.37 (1.25-1.51), <i>P</i> < 0.001]. When the survival analysis was stratified by mobility, no intergroup difference in prognosis was observed among patients with impaired mobility. However, among patients with independent mobility, patients in the Parkinson's disease group had a worse prognosis than those in the non- Parkinson's disease group [crude hazard ratio (95% confidence interval), 1.74 (1.42-2.13), <i>P</i> < 0.001]. Similar results were observed after propensity-score matching. Patients with cancer and comorbid Parkinson's disease had a worse prognosis than those without comorbid Parkinson's disease. The effect varied depending on mobility. These findings highlight the importance of carefully managing Parkinson's disease symptoms and maintaining mobility in cancer patients with Parkinson's disease, as this could potentially improve their prognosis and survival outcomes.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf347"},"PeriodicalIF":4.5,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12492484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234467","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":"Optic ataxia in patients with thalamic lesions.","authors":"Melanie Wilke, Hanna J Eisenberg, Carsten Schmidt-Samoa, Shirin Mahdavi, Igor Kagan, Peter Dechent, Jan Liman, Hans-Otto Karnath, Mathias Bähr","doi":"10.1093/braincomms/fcaf359","DOIUrl":"10.1093/braincomms/fcaf359","url":null,"abstract":"<p><p>Lesions in the parietal cortex can strongly impair visually guided reach-grasping behaviour. A specific reaching deficit termed 'optic ataxia' (OA) occurs when eye and hand position are dissociated. OA has typically been studied in patients with lesions in the parietal cortex, neglecting potential thalamic contributions. Here, we examined 28 acute stroke patients (age 58.9 ± 12.6 years) with circumscribed thalamic lesions for the presence of OA. We leveraged MRI-based lesion-symptom mapping to address the contributions of specific thalamic nuclei to visually guided reaching deficits under foveal and peripheral viewing conditions. Based on the cortical literature, we hypothesized that lesions in thalamic nuclei with strong connections to the inferior and superior parietal cortex, such as the ventrolateral nucleus and pulvinar might lead to OA. In comparison with age-matched healthy subjects (<i>n</i> = 40, age 60.6 ± 9.1 years), we identified five thalamic patients with OA, most pronounced for reaches with the contralesional hand into the contralesional space. While motor and grasping deficits and OA occurred frequently together, they did not always co-occur, and visual attention deficits could not account for the OA either. Comparing the lesion maps of patients with and without OA, the critical lesion site for OA was not restricted to one circumscribed thalamic region within the Morel atlas. Instead, it encompassed several medial and lateral nuclei within and around the internal medullary laminar complex. Interestingly, this region matches the so-called central thalamus, a functionally defined thalamic region that is considered a 'higher-order' nucleus complex. It receives afferent inputs from the cerebellum and brainstem regions and connects to fronto-parietal regions involved in eye movement control. Taken together, our results suggest the critical importance of thalamic nuclei for the spatial transformation from eye- into body-centred coordinates.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf359"},"PeriodicalIF":4.5,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12484446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214608","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":"Cell-weighted polygenic risk scores are associated with β-amyloid and tau biomarkers in Alzheimer's disease.","authors":"Atul Kumar, Alexa Pichet Binette, Divya Bali, Shorena Janelidze, Erik Stomrud, Sebastian Palmqvist, Jacob W Vogel, Oskar Hansson, Niklas Mattsson-Carlgren","doi":"10.1093/braincomms/fcaf353","DOIUrl":"10.1093/braincomms/fcaf353","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The molecular pathways influencing the build-up of β-amyloid and tau pathology in Alzheimer's disease are unclear. To investigate how the involvement of different cell types influences β-amyloid and tau, we utilized single-cell RNA-seq data to derive cell-weighted polygenic risk scores. We included participants from the BioFINDER-1 study, including cognitively unimpaired (&lt;i&gt;N&lt;/i&gt; = 734) individuals and patients with mild cognitive impairment (&lt;i&gt;N&lt;/i&gt; = 235), Alzheimer's diseasedementia (&lt;i&gt;N&lt;/i&gt; = 97) or non-Alzheimer's disease neurodegenerative diseases (&lt;i&gt;N&lt;/i&gt; = 227). We developed seven polygenic risk scores, including six cell-weighted (for astrocytes, excitatory neurons, inhibitory neurons, microglia, oligodendrocyte precursor cells and oligodendrocytes) and one full polygenic risk score without cell specificity. For each of the polygenic risk score models, we calculated seven scores (polygenic risk score 1-7) based on different &lt;i&gt;P&lt;/i&gt;-value thresholds (ranging from &lt;i&gt;P&lt;/i&gt;-value &lt; 0.05 to &lt;i&gt;P&lt;/i&gt;-value &lt; 5e-08) of variants from an independent large Alzheimer's disease genome-wide association study. We tested associations between the polygenic risk scores with β-amyloid [using cerebrospinal fluid (CSF) β-amyloid&lt;sub&gt;1-42&lt;/sub&gt;/β-amyloid&lt;sub&gt;1-40&lt;/sub&gt;], tau (using CSF pTau217) and cognitive measures (Mini-Mental State Examination score and Preclinical Alzheimer Cognitive Composite) using regression models adjusting for age, sex and the top genotype principal components. We also replicated the polygenic risk score association with β-amyloid (CSF β-amyloid&lt;sub&gt;1-42&lt;/sub&gt;/β-amyloid&lt;sub&gt;1-40&lt;/sub&gt;) and tau (CSF pTau217) in an independent cohort (BioFINDER-2), including cognitively unimpaired (&lt;i&gt;N&lt;/i&gt; = 773) individuals and patients with mild cognitive impairment (&lt;i&gt;N&lt;/i&gt; = 358), Alzheimer's disease dementia (&lt;i&gt;N&lt;/i&gt; = 286) or non-Alzheimer's disease neurodegenerative diseases (&lt;i&gt;N&lt;/i&gt; = 319). We observed differential cellular effects on β-amyloid, pTau217 and cognitive measures. There are substantial effects of neuronal-specific polygenic risk scores on β-amyloid, pTau217 and cognitive measures. The microglial-polygenic risk scores showed more significant effects on pTau217 than on β-amyloid. β-Amyloid positivity partly mediated the associations between polygenic risk scores and pTau217, with the lowest mediation effect observed for the microglial-polygenic risk scores (on average 33%). Cell-weighted gene expression has differential effects on pathological β-amyloid and tau metabolism, as well as cognitive decline. Cell-weighted gene expression related to microglia is preferentially relevant for the metabolism of soluble phosphorylated tau through partly β-amyloid-independent mechanisms. Cell-weighted gene expression related to neurons shows the strongest associations with cognition. These findings inform further studies that address specific cell types for various aspects of Alzheimer's disease, including the development of nov","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf353"},"PeriodicalIF":4.5,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12484444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214750","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":"Sulcal morphology in former American football players.","authors":"Leonard B Jung, Anya S Mirmajlesi, Jared Stearns, Katherine Breedlove, Omar John, Nicholas Kim, Alana Wickham, Yi Su, Hillary Protas, Zachary H Baucom, Fatima Tuz-Zahra, Yorghos Tripodis, Daniel H Daneshvar, Tim L T Wiegand, Tashrif Billah, Ofer Pasternak, Carina Heller, Brian S Im, Shae Datta, Michael J Coleman, Charles H Adler, Charles Bernick, Laura J Balcer, Michael L Alosco, Alexander P Lin, Jeffrey L Cummings, Eric M Reiman, Robert A Stern, Martha E Shenton, Sylvain Bouix, Inga K Koerte, Hector Arciniega","doi":"10.1093/braincomms/fcaf345","DOIUrl":"10.1093/braincomms/fcaf345","url":null,"abstract":"<p><p>Repetitive head impacts are associated with structural brain changes and an increased risk for chronic traumatic encephalopathy, a progressive neurodegenerative disease that can only be diagnosed after death. Chronic traumatic encephalopathy is defined by the abnormal accumulation of phosphorylated tau protein, particularly at the depths of the superior frontal sulci, suggesting that sulcal morphology may serve as a relevant structural biomarker. Contact sport athletes, such as former football players, are at elevated risk due to their prolonged exposure to repetitive head impacts. Cortical atrophy linked to underlying tau accumulation may result in shallower and wider sulci, potentially making sulcal morphology an imaging marker for identifying individuals at risk for this disease. This study investigated sulcal morphological differences in former football players and examined associations with age, football-related exposure, clinical diagnosis of traumatic encephalopathy syndrome, levels of certainty for chronic traumatic encephalopathy pathology, neuropsychological performance, and positron emission tomography imaging using flortaucipir. We analysed structural magnetic resonance imaging data from 169 male former football players (mean age 57.2 (8.2) years, range 45-74) and 54 age-matched, unexposed asymptomatic male controls (mean age 59.4 (8.5) years, range 45-74). Sulcal depth and width were quantified using the CalcSulc, focusing on two regions in each hemisphere commonly affected by chronic traumatic encephalopathy pathology: the superior frontal and occipitotemporal sulci. Generalized least squares models were used to assess group differences and interactions with age and football exposure variables, including age of first exposure, total years played, and cumulative head impact exposure. An analysis of covariance evaluated relationships between sulcal morphology, clinical measures, and flortaucipir uptake, adjusting for age, race, body mass index, education, imaging site, apolipoprotein E4 status, and total intracranial volume. Former football players demonstrated significantly shallower sulcal depth in the left superior frontal sulcus compared to unexposed controls. Earlier age of first exposure and longer football careers were associated with greater widening of the left occipitotemporal sulcus. Higher cumulative head impact exposure was linked to reduced sulcal depth in the left superior frontal region. However, sulcal morphology was not associated with clinical diagnosis, levels of certainty, neuropsychological test performance, or flortaucipir imaging. These findings suggest that sulcal morphology may reflect cumulative exposure to repetitive head impacts, particularly in brain regions vulnerable to chronic traumatic encephalopathy pathology. Future ante- and post-mortem validation studies are needed to determine whether sulcal morphology can serve as a reliable <i>in vivo</i> biomarker of risk.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf345"},"PeriodicalIF":4.5,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12492488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234425","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":"More than chronic pain: behavioural and psychosocial protective factors predict lower brain age in adults with/at risk of knee osteoarthritis over two years.","authors":"Jared J Tanner, Angela Mickle, Udell Holmes, Brittany Addison, Kenia Rangel, Cynthia Garvan, Roland Staud, Song Lai, David Redden, Burel R Goodin, Catherine C Price, Roger B Fillingim, Kimberly T Sibille","doi":"10.1093/braincomms/fcaf344","DOIUrl":"10.1093/braincomms/fcaf344","url":null,"abstract":"<p><p>The interplay between chronic musculoskeletal pain and brain ageing is complex. Studies employing machine learning models to assess relationships between brain age and chronic pain generally show that higher chronic pain severity associates with older brain age. Analyses to date have not considered individual and community-level socioenvironmental risk factors or behavioural/psychosocial protective factors as potential modifiers of cross-sectional and longitudinal brain age. This study aimed to elucidate the relationships between chronic pain, socioenvironmental risk, behavioural/psychosocial protective factors, and brain ageing. The sample comprised 197 adults (Men:Women = 68:129) from a prospective observational cohort study. Most individuals reported knee pain and were with/at risk of osteoarthritis. A subset of 128 participants (Men:Women = 41:87) completed a follow-up MRI session at 2 years and were included in the longitudinal analysis (Aim 2). Participants were 45-85 years of age and self-identified as non-Hispanic Black or non-Hispanic White. Data collected included demographics, health history, pain assessments, individual and community-level socioenvironmental factors (education, income, household size, marital and insurance status, and area deprivation index) coded as a summative socioenvironmental risk variable, and behavioural/psychosocial factors (tobacco use, waist circumference, optimism, positive and negative affect, perceived stress, perceived social support, sleep) coded as a summative behavioural/psychosocial protective factor variable. Structural MRI data were used to estimate brain age by applying a machine learning approach (DeepBrainNet). Cross-sectional analyses utilized regression and analysis of variance, while longitudinal analyses utilized a linear mixed model. Higher chronic pain stage and socioenvironmental risk are associated with an increased brain age gap (the difference between chronological age and predicted brain age). Participants who had higher socioenvironmental risk had brains that were about three years older than those of participants with lower risk. Having more behavioural/psychosocial protective factors correlated with a lower brain age gap; participants with higher behavioural/psychosocial protective factors had brains that were over three years younger than participants with fewer behavioural/psychosocial protective factors. Longitudinally, higher baseline behavioural/psychosocial protective factors are associated with lower brain age over the 2-year span, beyond the effects of chronic pain stage and socioenvironmental risk. Our findings show behavioural/psychosocial protective factors may counteract neurobiological ageing and help buffer the brain from chronic pain.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf344"},"PeriodicalIF":4.5,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12465110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187481","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":"Left-hemisphere glioma drives systematic patterns of contralesional functional connectivity.","authors":"Emma Strawderman, Frank E Garcea, Madalina E Tivarus, Steven P Meyers, Adnan A Hirad, William M Burns, Kevin A Walter, Tyler Schmidt, Webster H Pilcher, Bradford Z Mahon","doi":"10.1093/braincomms/fcaf349","DOIUrl":"10.1093/braincomms/fcaf349","url":null,"abstract":"<p><p>Gliomas can cause changes in functional networks both proximal and distal to the lesion. Understanding glioma-induced functional reorganization has implications for understanding variability across patients in cognitive outcomes, disease progression, and survival. Here, we leverage machine learning techniques to show that left-hemisphere gliomas are associated with systematic changes in right-hemisphere connectivity. We analyzed right-hemisphere functional connectivity patterns from resting-state functional MRI in 48 patients with left-hemisphere gliomas (mean age 50 years, 31 males) and 107 neurotypical controls (mean age 49 years, 44 males). We employed machine learning techniques, including support vector machines, to assess whether the pattern of right-hemispheric resting-state functional connectivity could distinguish left-hemisphere glioma patients from controls, and predict glioma characteristics, including isocitrate dehydrogenase mutation, World Health Organization grade, and relative size. A support vector machine binary classifier distinguished patients from controls based on right-hemisphere connectivity with 89% accuracy and 84% precision (both <i>P</i> = 0.001), indicating consistent contralesional connectivity differences as a function of glioma. The model also achieved 79% sensitivity for detecting patients (<i>P</i> = 0.028). Furthermore, patients with similar right-hemisphere connectivity profiles had lesions in similar locations within the left hemisphere, suggesting that the observed connectivity changes are influenced by glioma location. Additionally, the pattern of right-hemisphere connectivity could predict the presence of left-hemisphere gliomas specifically in regions of the parietal lobe. We also found that distinct contralesional connectivity patterns classified glioma molecular subtypes, achieving 78% accuracy in classifying patients by isocitrate dehydrogenase mutation (<i>P</i> = 0.004), with 82% precision (<i>P</i> = 0.003) and 73% sensitivity (<i>P</i> = 0.048) for mutant-tumors. However, right-hemisphere functional connectivity could not distinguish patients based on their tumor grade or relative size, with models performing no different from chance. These findings provide evidence for systematic changes in the contralesional connectome in glioma patients, consistent with theories of glioma-induced functional reorganization. This highlights the right hemisphere's role in adaptive responses to left-hemispheric gliomas and further underscores the importance of molecular profiling and tumor location in understanding reorganization potential.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf349"},"PeriodicalIF":4.5,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12464944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187950","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":"Thalamus anatomy predicts cognitive performance and hippocampal atrophy in aging adults: a UK Biobank study.","authors":"Guocheng Jiang, Fa-Hsuan Lin, Hugo Cogo-Moreira, Jennifer S Rabin, J Jean Chen, Walter Swardfager, Bradley J MacIntosh","doi":"10.1093/braincomms/fcaf334","DOIUrl":"10.1093/braincomms/fcaf334","url":null,"abstract":"<p><p>The thalamus has extensive inter-connectedness with different brain regions in serving cognitive processes. In a community-dwelling aging population from the United Kingdom, this study examined the independent contribution of thalamus volume loss to cognitive performances and the longitudinal anatomical relationship between the thalamus and the interconnected hippocampus. We accessed MRI data from 4348 cognitively unimpaired older adults from the UK Biobank, of whom 653 participants had follow-up MRI. We estimated regional brain volumes using T1-weighted MRI. Linear models tested the association between the thalamus volume and a cognitive composite score derived from digit-symbol substitution and trail-making tests. We used latent change score models to test the longitudinal associations between thalamus volume at baseline and the trajectory of hippocampal atrophy, and vice versa. Baseline thalamus volume was positively associated with the cognitive composite score ( <math><mi>β</mi> <mo>=</mo> <mn>0.055</mn> <mo>±</mo> <mn>0.018</mn></math> , <i>P</i> = 0.002, <i>R</i> ² = 0.09). A larger baseline thalamus volume predicted slower hippocampal atrophy ( <math><msub><mi>γ</mi> <mrow><mi>T</mi> <mo>→</mo> <mrow><mi>dH</mi></mrow> </mrow> </msub> <mo>=</mo> <mo>-</mo> <mn>0.048</mn> <mo>±</mo> <mn>0.015</mn> <mo>,</mo> <mspace></mspace> <mi>P</mi> <mo>=</mo> <mn>0.001</mn> <mo>,</mo> <mspace></mspace> <mspace></mspace> <msup><mi>R</mi> <mn>2</mn></msup> <mo>=</mo> <mn>0.09</mn></math> ), while larger hippocampal volume at baseline predicted faster thalamic atrophy ( <math><msub><mi>γ</mi> <mrow><mi>H</mi> <mo>→</mo> <mi>d</mi> <mi>T</mi></mrow> </msub> <mo>=</mo> <mn>0.043</mn> <mo>±</mo> <mn>0.022</mn> <mo>,</mo> <mspace></mspace> <mi>P</mi> <mo>=</mo> <mn>0.048</mn> <mo>,</mo> <mspace></mspace> <msup><mi>R</mi> <mn>2</mn></msup> <mo>=</mo> <mn>0.04</mn></math> ). Sex-stratified analysis revealed that hippocampal volume significantly predicted thalamic atrophy only in women. This study revealed that thalamic volume loss was associated with impaired processing speed and executive function. Thalamus and hippocampus anatomy showed bidirectional longitudinal associations and demonstrated sex differences. These findings underscore the thalamus anatomy as an important marker of brain health in the aging population.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf334"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139752","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":"Local field potential signal transmission is correlated with the fractional anisotropy measured by diffusion tractography.","authors":"Maral Kasiri, Sumiko Abe, Rahil Soroushmojdehi, Estefania Hernandez-Martin, Seyyed Alireza Seyyed Mousavi, Terence D Sanger","doi":"10.1093/braincomms/fcaf336","DOIUrl":"10.1093/braincomms/fcaf336","url":null,"abstract":"<p><p>In this paper we aim to examine the correlation between diffusion tensor imaging parameters of anatomical connectivity and characteristics of signal transmission obtained from patient-specific transfer function models. Here, we focused on elucidating the correlation between structural and functional neural connectivity within a cohort of pediatric patients diagnosed with dystonia. Diffusion tractography images were obtained from 12 patients with dystonia prior to the deep brain stimulation surgery. For each patient, we processed the imaging data to estimate anatomical measures including fractional anisotropy, axial diffusivity, number of fibre tracts per unit area, and fibre tract length. After the implantation of temporary depth leads for each patient as part of their treatment plan, intracranial signals were recorded. Transfer function models of local field potential recordings and the corresponding measures of functional connectivity were computed for each patient. Linear mixed effect analysis was then employed to determine the relationship between transfer function measures and diffusion tractography parameters. Our results illustrate a positive correlation between fractional anisotropy, AD, and intrinsic neural transmission measures, representing amplification and spread of intrinsic neural oscillations, obtained from the transfer functions models. However, no significant correlation was found between the functional connectivity and number of fibre tracts or fibre lengths. Our findings suggest that white matter integrity, as measured by fractional anisotropy and AD, can potentially reflect the amplification and spread of intrinsic brain signals throughout the network. This study underscores the significant relationship between structural and functional connectivity, offering valuable insights into propagation of neural activity in the brain network and potential implications for optimizing non-invasive treatments and planning for neurological disorders.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 5","pages":"fcaf336"},"PeriodicalIF":4.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115177","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}