Brain communications最新文献

{"title":"No evidence of altered language laterality in people who stutter across different brain imaging studies of speech and language.","authors":"Birtan Demirel, Jennifer Chesters, Emily L Connally, Patricia M Gough, David Ward, Peter Howell, Kate E Watkins","doi":"10.1093/braincomms/fcae305","DOIUrl":"10.1093/braincomms/fcae305","url":null,"abstract":"<p><p>A long-standing neurobiological explanation of stuttering is the incomplete cerebral dominance theory, which refers to competition between two hemispheres for 'dominance' over handedness and speech, causing altered language lateralization. Renewed interest in these ideas came from brain imaging findings in people who stutter of increased activity in the right hemisphere during speech production or of shifts in activity from right to left when fluency increased. Here, we revisited this theory using functional MRI data from children and adults who stutter, and typically fluent speakers (119 participants in total) during four different speech and language tasks: overt sentence reading, overt picture description, covert sentence reading and covert auditory naming. Laterality indices were calculated for the frontal and temporal lobes using the laterality index toolbox running in Statistical Parametric Mapping. We also repeated the analyses with more specific language regions, namely the pars opercularis (Brodmann area 44) and pars triangularis (Brodmann area 45). Laterality indices in people who stutter and typically fluent speakers did not differ, and Bayesian analyses provided moderate to anecdotal levels of support for the null hypothesis (i.e. no differences in laterality in people who stutter compared with typically fluent speakers). The proportions of the people who stutter and typically fluent speakers who were left lateralized or had atypical rightward or bilateral lateralization did not differ. We found no support for the theory that language laterality is reduced or differs in people who stutter compared with typically fluent speakers.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae305"},"PeriodicalIF":4.1,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11430911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142334344","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":"Metric comparison of connectome-based lesion-symptom mapping in post-stroke aphasia.","authors":"Junhua Ding, Melissa Thye, Amelia J Edmondson-Stait, Jerzy P Szaflarski, Daniel Mirman","doi":"10.1093/braincomms/fcae313","DOIUrl":"10.1093/braincomms/fcae313","url":null,"abstract":"<p><p>Connectome-based lesion-symptom mapping relates behavioural impairments to disruption of structural brain connectivity. Connectome-based lesion-symptom mapping can be based on different approaches (diffusion MRI versus lesion mask), network scales (whole brain versus regions of interest) and measure types (tract-based, parcel-based, or network-based metrics). We evaluated the similarity of different connectome-based lesion-symptom mapping processing choices and identified factors that influence the results using multiverse analysis-the strategy of conducting and displaying the results of all reasonable processing choices. Metrics derived from lesion masks and diffusion-weighted images were tested for association with Boston Naming Test and Token Test performance in a sample of 50 participants with aphasia following left hemispheric stroke. 'Direct' measures were derived from diffusion-weighted images. 'Indirect' measures were derived by overlaying lesion masks on a white matter atlas. Parcel-based connectomes were constructed for the whole brain and regions of interest (14 language-relevant parcels). Numerous tract-based and network-based metrics were calculated. There was a high discrepancy across processing approaches (diffusion-weighted images versus lesion masks), network scales (whole brain versus regions of interest) and metric types. Results indicate weak correlations and different connectome-based lesion-symptom mapping results across the processing choices. Substantial methodological work is needed to validate the various decision points that arise when conducting connectome-based lesion-symptom mapping analyses. Multiverse analysis is a useful strategy for evaluating the similarity across different processing choices in connectome-based lesion-symptom mapping.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae313"},"PeriodicalIF":4.1,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142334343","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 glycogen build-up measured by magnetic resonance spectroscopy in classic infantile Pompe disease.","authors":"Chloé Najac, Nadine A M E van der Beek, Vincent O Boer, Pieter A van Doorn, Ans T van der Ploeg, Itamar Ronen, Hermien E Kan, Johanna M P van den Hout","doi":"10.1093/braincomms/fcae303","DOIUrl":"10.1093/braincomms/fcae303","url":null,"abstract":"<p><p>Classic infantile Pompe disease is caused by abnormal lysosomal glycogen accumulation in multiple tissues, including the brain due to a deficit in acid α-glucosidase. Although treatment with recombinant human acid α-glucosidase has dramatically improved survival, recombinant human acid α-glucosidase does not reach the brain, and surviving classic infantile Pompe patients develop progressive cognitive deficits and white matter lesions. We investigated the feasibility of measuring non-invasively glycogen build-up and other metabolic alterations in the brain of classic infantile Pompe patients. Four classic infantile patients (8-16 years old) and 4 age-matched healthy controls were scanned on a 7 T MRI scanner. We used T₂-weighted MRI to assess the presence of white matter lesions as well as ¹H magnetic resonance spectroscopy and magnetic resonance spectroscopy imaging to obtain the neurochemical profile and its spatial distribution, respectively. All patients had widespread white matter lesions on T₂-weighted images. Magnetic resonance spectroscopy data from a single volume of interest positioned in the periventricular white matter showed a clear shift in the neurochemical profile, particularly a significant increase in glycogen (result of acid α-glucosidase deficiency) and decrease in <i>N</i>-acetyl-aspartate (marker of neuronal damage) in patients. Magnetic resonance spectroscopy imaging results were in line and showed a widespread accumulation of glycogen and a significant lower level of <i>N</i>-acetyl-aspartate in patients. Our results illustrate the unique potential of ¹H magnetic resonance spectroscopy (imaging) to provide a non-invasive readout of the disease pathology in the brain. Further study will assess its potential to monitor disease progression and the correlation with cognitive decline.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae303"},"PeriodicalIF":4.1,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303360","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":"Investigating recovery after a spontaneous intracerebral haemorrhage in zebrafish larvae.","authors":"Siobhan Crilly, Isabel Shand, Abigail Bennington, Emily McMahon, Daisy Flatman, Victor S Tapia, Paul R Kasher","doi":"10.1093/braincomms/fcae310","DOIUrl":"https://doi.org/10.1093/braincomms/fcae310","url":null,"abstract":"<p><p>Intracerebral haemorrhage is a debilitating stroke sub-type with high morbidity and mortality rates. For survivors, rehabilitation is a long process, and with no available therapeutics to limit the immediate pathophysiology of the haemorrhage, recovery is dependent on individual neuroplasticity. We have previously shown that zebrafish larvae can be used to model spontaneous brain haemorrhage. Zebrafish exhibit innate recovery mechanisms and are often used as a model system for investigation into regeneration after injury, including injury to the nervous system. Here, we investigate the spontaneous and immediate recovery in zebrafish larvae following an intracerebral haemorrhage at 2 days post-fertilisation, during pre-protected stages and over the first 3 weeks of life. We have shown that following the onset of bleed at ∼2 days post-fertilisation zebrafish are capable of clearing the haematoma through the ventricles. Brain cell damage associated with intracerebral haemorrhage is resolved within 48 h, and this recovery is associated with survival rates equal to wildtype and non-haemorrhaged sibling control animals. Larvae express more nestin-positive neural progenitor cells 24 h after injury when the most damage is observed, and through mass spectrometry analysis, we have determined that these cells are highly proliferative and may specially differentiate into oligodendrocytes. This study provides an insight into the haematoma resolution processes in a live, intact organism, and may suggest potential therapeutic approaches to support the recovery of intracerebral haemorrhage patients.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae310"},"PeriodicalIF":4.1,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11483570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483043","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":"Causal relationships of grey matter structures in multiple sclerosis and neuromyelitis optica spectrum disorder: insights from Mendelian randomization.","authors":"Jie Sun, Yingying Xie, Tongli Li, Yunfei Zhao, Wenjin Zhao, Zeyang Yu, Shaoying Wang, Yujie Zhang, Hui Xue, Yayuan Chen, Zuhao Sun, Zhang Zhang, Yaou Liu, Ningnannan Zhang, Feng Liu","doi":"10.1093/braincomms/fcae308","DOIUrl":"https://doi.org/10.1093/braincomms/fcae308","url":null,"abstract":"<p><p>Multiple sclerosis and neuromyelitis optica spectrum disorder are two debilitating inflammatory demyelinating diseases of the CNS. Although grey matter alterations have been linked to both multiple sclerosis and neuromyelitis optica spectrum disorder in observational studies, it is unclear whether these associations indicate causal relationships between these diseases and grey matter changes. Therefore, we conducted a bidirectional two-sample Mendelian randomization analysis to investigate the causal relationships between 202 grey matter imaging-derived phenotypes (33 224 individuals) and multiple sclerosis (47 429 cases and 68 374 controls) as well as neuromyelitis optica spectrum disorder (215 cases and 1244 controls). Our results suggested that genetically predicted multiple sclerosis was positively associated with the surface area of the left parahippocampal gyrus (<i>β</i> = 0.018, <i>P</i> = 2.383 × 10^-4) and negatively associated with the volumes of the bilateral caudate (left: <i>β</i> = -0.020, <i>P</i> = 7.203 × 10^-5; right: <i>β</i> = -0.021, <i>P</i> = 3.274 × 10^-5) and putamen nuclei (left: <i>β</i> = -0.030, <i>P</i> = 2.175 × 10^-8; right: <i>β</i> = -0.024, <i>P</i> = 1.047 × 10^-5). In addition, increased neuromyelitis optica spectrum disorder risk was associated with an increased surface area of the left paracentral gyrus (<i>β</i> = 0.023, <i>P</i> = 1.025 × 10^-4). Conversely, no evidence was found for the causal impact of grey matter imaging-derived phenotypes on disease risk in the opposite direction. We provide suggestive evidence that genetically predicted multiple sclerosis and neuromyelitis optica spectrum disorder are associated with increased cortical surface area and decreased subcortical volume in specific regions. Our findings shed light on the associations of grey matter alterations with the risk of multiple sclerosis and neuromyelitis optica spectrum disorder.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae308"},"PeriodicalIF":4.1,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142334339","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":"Understanding the mechanisms of fatigue in multiple sclerosis: linking interoception, metacognition and white matter dysconnectivity.","authors":"Iulia Danciut, Charlotte L Rae, Waqar Rashid, James Scott, Marco Bozzali, Mihaela Iancu, Sarah N Garfinkel, Samira Bouyagoub, Nicholas G Dowell, Dawn Langdon, Mara Cercignani","doi":"10.1093/braincomms/fcae292","DOIUrl":"https://doi.org/10.1093/braincomms/fcae292","url":null,"abstract":"<p><p>One of the most prominent symptoms in multiple sclerosis is pathological fatigue, often described by sufferers as one of the most debilitating symptoms, affecting quality of life and employment. However, the mechanisms of both, physical and cognitive fatigue in multiple sclerosis remain elusive. Here, we use behavioural tasks and quantitative MRI to investigate the neural correlates of interoception (the ability to sense internal bodily signals) and metacognition (the ability of the brain to assess its own performance), in modulating cognitive fatigue. Assuming that structural damage caused by multiple sclerosis pathology might impair the neural pathways subtending interoception and/or metacognition, we considered three alternative hypotheses to explain fatigue as a consequence of, respectively: (i) reduced interoceptive accuracy, (ii) reduced interoceptive insight or (iii) reduced global metacognition. We then explored associations between these behavioural measures and white matter microstructure, assessed by diffusion and magnetisation transfer MRI. Seventy-one relapsing-remitting multiple sclerosis patients participated in this cross-sectional study (mean age 43, 62% female). Patient outcomes relevant for fatigue were measured, including disability, disease duration, depression, anxiety, sleepiness, cognitive function, disease modifying treatment and quality of life. Interoceptive and metacognitive parameters were measured using heartbeat tracking and discrimination tasks, and metacognitive visual and memory tasks. MRI was performed in 69 participants, including diffusion tensor MRI, neurite orientation dispersion and density imaging and quantitative magnetisation transfer. Associations between interoception and metacognition and the odds of high cognitive fatigue were tested by unconditional binomial logistic regression. The odds of cognitive fatigue were higher in the people with low interoceptive insight (<i>P</i> = 0.03), while no significant relationships were found between fatigue and other interoceptive or metacognitive parameters, suggesting a specific impairment in interoceptive metacognition, rather than interoception generally, or metacognition generally. Diffusion MRI-derived fractional anisotropy and neurite density index showed significant (<i>P</i> < 0.05) negative associations with cognitive fatigue in a widespread bilateral white matter network. Moreover, there was a significant (<i>P</i> < 0.05) interaction between cognitive fatigue and interoceptive insight, suggesting that the poorer the white matter structure, the lower the interoceptive insight, and the worse the fatigue. The results point towards metacognitive impairment confined to the interoceptive domain, in relapsing-remitting patients with cognitive fatigue. The neural basis of this impairment is supported by a widespread white matter network in which loss of neurite density plays a role.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae292"},"PeriodicalIF":4.1,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11406465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303346","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":"3T sodium-MRI as predictor of neurocognition in nondemented older adults: a cross sectional study.","authors":"Elaine Lui, Vijay K Venkatraman, Sue Finch, Michelle Chua, Tie-Qiang Li, Bradley P Sutton, Christopher E Steward, Bradford Moffat, Elizabeth V Cyarto, Kathryn A Ellis, Christopher C Rowe, Colin L Masters, Nicola T Lautenschlager, Patricia M Desmond","doi":"10.1093/braincomms/fcae307","DOIUrl":"https://doi.org/10.1093/braincomms/fcae307","url":null,"abstract":"<p><p>Dementia is a burgeoning global problem. Novel magnetic resonance imaging (MRI) metrics beyond volumetry may bring new insight and aid clinical trial evaluation of interventions early in the Alzheimer's disease course to complement existing imaging and clinical metrics. To determine whether: (i) normalized regional sodium-MRI values (Na-SI) are better predictors of neurocognitive status than volumetry (ii) cerebral amyloid PET status improves modelling. Nondemented older adult (>60 years) volunteers of known Alzheimer's Disease Assessment Scale (ADAS-Cog11), Mini-Mental State Examination (MMSE) and Consortium to Establish a Registry for Alzheimer's Disease (CERAD) neurocognitive test scores, ApolipoproteinE (APOE) e4 +/- cerebral amyloid PET status were prospectively recruited for 3T sodium-MRI brain scans. Left and right hippocampal, entorhinal and precuneus volumes and Na-SI (using the proportional intensity scaling normalization method with field inhomogeneity and partial volume corrections) were obtained after segmentation and co-registration of 3D-T1-weighted proton images. Descriptive statistics, correlation and best-subset regression analyses were performed. In our 76 nondemented participants (mean(standard deviation) age 75(5) years; woman 47(62%); cognitively unimpaired 54/76(71%), mildly cognitively impaired 22/76(29%)), left hippocampal Na-SI, not volume, was preferentially in the best models for predicting MMSE (Odds Ratio (OR) = 0.19(Confidence Interval (CI) = 0.07,0.53), <i>P</i>-value = 0.001) and ADAS-Cog11 (Beta(B) = 1.2(CI = 0.28,2.1), <i>P</i>-value = 0.01) scores. In the entorhinal analysis, right entorhinal Na-SI, not volume, was preferentially selected in the best model for predicting ADAS-Cog11 (B = 0.94(CI = 0.11,1.8), <i>P</i>-value = 0.03). While right entorhinal Na-SI and volume were both selected for MMSE modelling (Na-SI OR = 0.23(CI = 0.09,0.6), <i>P</i>-value = 0.003; volume OR = 2.6(CI = 1.0,6.6), <i>P</i>-value = 0.04), independently, Na-SI explained more of the variance (Na-SI <i>R</i> ² = 10.3; volume <i>R</i> ² = 7.5). No imaging variable was selected in the best CERAD models. Adding cerebral amyloid status improved model fit (Akaike Information Criterion increased 2.0 for all models, <i>P</i>-value < 0.001-0.045). Regional Na-SI were more predictive of MMSE and ADAS-Cog11 scores in our nondemented older adult cohort than volume, hippocampal more robust than entorhinal region of interest. Positive amyloid status slightly further improved model fit.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae307"},"PeriodicalIF":4.1,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142334338","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 influence of temperature and genomic variation on intracranial EEG measures in people with epilepsy.","authors":"Olivia C McNicholas, Diego Jiménez-Jiménez, Joana F A Oliveira, Lauren Ferguson, Ravishankara Bellampalli, Charlotte McLaughlin, Fahmida Amin Chowdhury, Helena Martins Custodio, Patrick Moloney, Anna Mavrogianni, Beate Diehl, Sanjay M Sisodiya","doi":"10.1093/braincomms/fcae269","DOIUrl":"10.1093/braincomms/fcae269","url":null,"abstract":"<p><p>Heatwaves have serious impacts on human health and constitute a key health concern from anthropogenic climate change. People have different individual tolerance for heatwaves or unaccustomed temperatures. Those with epilepsy may be particularly affected by temperature as the electroclinical hallmarks of brain excitability in epilepsy (inter-ictal epileptiform discharges and seizures) are influenced by a range of physiological and non-physiological conditions. Heatwaves are becoming more common and may affect brain excitability. Leveraging spontaneous heatwaves during periods of intracranial EEG recording in participants with epilepsy in a non-air-conditioned telemetry unit at the National Hospital for Neurology and Neurosurgery in London from May to August 2015-22, we examined the impact of heatwaves on brain excitability. In London, a heatwave is defined as three or more consecutive days with daily maximum temperatures ≥28°C. For each participant, we counted inter-ictal epileptiform discharges using four 10-min segments within, and outside of, heatwaves during periods of intracranial EEG recording. Additionally, we counted all clinical and subclinical seizures within, and outside of, heatwaves. We searched for causal rare genetic variants and calculated the epilepsy PRS. Nine participants were included in the study (six men, three women), median age 30 years (range 24-39). During heatwaves, there was a significant increase in the number of inter-ictal epileptiform discharges in three participants. Five participants had more seizures during the heatwave period, and as a group, there were significantly more seizures during the heatwaves. Genetic data, available for eight participants, showed none had known rare, genetically-determined epilepsies, whilst all had high polygenic risk scores for epilepsy. For some people with epilepsy, and not just those with known, rare, temperature-sensitive epilepsies, there is an association between heatwaves and increased brain excitability. These preliminary data require further validation and exploration, as they raise concerns about the impact of heatwaves directly on brain health.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae269"},"PeriodicalIF":4.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11383581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303345","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":"Changes in electrophysiological aperiodic activity during cognitive control in Parkinson's disease.","authors":"Noémie Monchy, Julien Modolo, Jean-François Houvenaghel, Bradley Voytek, Joan Duprez","doi":"10.1093/braincomms/fcae306","DOIUrl":"https://doi.org/10.1093/braincomms/fcae306","url":null,"abstract":"<p><p>Cognitive symptoms in Parkinson's disease are common and can significantly affect patients' quality of life. Therefore, there is an urgent clinical need to identify a signature derived from behavioural and/or neuroimaging indicators that could predict which patients are at increased risk for early and rapid cognitive decline. Recently, converging evidence identified that aperiodic activity of the EEG reflects meaningful physiological information associated with age, development, cognitive and perceptual states or pathologies. In this study, we aimed to investigate aperiodic activity in Parkinson's disease during cognitive control and characterize its possible association with behaviour. Here, we recorded high-density EEG in 30 healthy controls and 30 Parkinson's disease patients during a Simon task. We analysed task-related behavioural data in the context of the activation-suppression model and extracted aperiodic parameters (offset, exponent) at both scalp and source levels. Our results showed lower behavioural performances in cognitive control as well as higher offsets in patients in the parieto-occipital areas, suggesting increased excitability in Parkinson's disease. A small congruence effect on aperiodic parameters in pre- and post-central brain areas was also found, possibly associated with task execution. Significant differences in aperiodic parameters between the resting-state, pre- and post-stimulus phases were seen across the whole brain, which confirmed that the observed changes in aperiodic activity are linked to task execution. No correlation was found between aperiodic activity and behaviour or clinical features. Our findings provide evidence that EEG aperiodic activity in Parkinson's disease is characterized by greater offsets, and that aperiodic parameters differ depending on arousal state. However, our results do not support the hypothesis that the behaviour-related differences observed in Parkinson's disease are related to aperiodic changes. Overall, this study highlights the importance of considering aperiodic activity contributions in brain disorders and further investigating the relationship between aperiodic activity and behaviour.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae306"},"PeriodicalIF":4.1,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11411214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303377","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":"Colchicine treatment in amyotrophic lateral sclerosis: safety, biological and clinical effects in a randomized clinical trial.","authors":"Giulia Gianferrari, Riccardo Cuoghi Costantini, Valeria Crippa, Serena Carra, Valentina Bonetto, Orietta Pansarasa, Cristina Cereda, Elisabetta Zucchi, Ilaria Martinelli, Cecilia Simonini, Roberto Vicini, Nicola Fini, Francesca Trojsi, Carla Passaniti, Nicola Ticozzi, Alberto Doretti, Luca Diamanti, Giuseppe Fiamingo, Amelia Conte, Eleonora Dalla Bella, Eustachio D'Errico, Eveljn Scarian, Laura Pasetto, Francesco Antoniani, Veronica Galli, Elena Casarotto, Roberto D'Amico, Angelo Poletti, Jessica Mandrioli","doi":"10.1093/braincomms/fcae304","DOIUrl":"https://doi.org/10.1093/braincomms/fcae304","url":null,"abstract":"<p><p>In preclinical studies, the anti-inflammatory drug colchicine, which has never been tested in amyotrophic lateral sclerosis, enhanced the expression of autophagy factors and inhibited accumulation of transactive response DNA-binding protein 43 kDa, a known histopathological marker of amyotrophic lateral sclerosis. This multicentre, randomized, double-blind trial enrolled patients with probable or definite amyotrophic lateral sclerosis who experienced symptom onset within the past 18 months. Patients were randomly assigned in a 1:1:1 ratio to receive colchicine at a dose of 0.005 mg/kg/day, 0.01 mg/kg/day or placebo for a treatment period of 30 weeks. The number of positive responders, defined as patients with a decrease lesser than 4 points in the Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised total score during the 30-week treatment period, was the primary outcome. Disease progression, survival, safety and quality of life at the end of treatment were the secondary clinical outcomes. Secondary biological outcomes included changes from baseline to treatment end of stress granule and autophagy responses, transactive response DNA-binding protein 43 kDa, neurofilament accumulation and extracellular vesicle secretion, between the colchicine and placebo groups. Fifty-four patients were randomized to receive colchicine (<i>n</i> = 18 for each colchicine arm) or placebo (<i>n</i> = 18). The number of positive responders did not differ between the placebo and colchicine groups: 2 out of 18 patients (11.1%) in the placebo group, 5 out of 18 patients (27.8%) in the colchicine 0.005 mg/kg/day group (odds ratio = 3.1, 97.5% confidence interval 0.4-37.2, <i>P</i> = 0.22) and 1 out of 18 patients (5.6%) in the colchicine 0.01 mg/kg/day group (odds ratio = 0.5, 97.5% confidence interval 0.01-10.2, <i>P</i> = 0.55). During treatment, a slower Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised decline was detected in patients receiving colchicine 0.005 mg/kg/day (mean difference = 0.53, 97.5% confidence interval 0.07-0.99, <i>P</i> = 0.011). Eight patients experienced adverse events in placebo arm (44.4%), three in colchicine 0.005 mg/kg/day (16.7%) and seven in colchicine 0.01 mg/kg/day arm (35.9%). The differences in adverse events were not statistically significant. In conclusion, colchicine treatment was safe for amyotrophic lateral sclerosis patients. Further studies are required to better understand mechanisms of action and clinical effects of colchicine in this condition.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"6 5","pages":"fcae304"},"PeriodicalIF":4.1,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11406549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142303379","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}