Brain communications最新文献

{"title":"Multimodal deep learning model for prediction of prognosis in central nervous system inflammation.","authors":"Bo Kyu Choi, Yoonhyeok Choi, Sooyoung Jang, Woo-Seok Ha, Soomi Cho, Kimoon Chang, Beomseok Sohn, Kyung Min Kim, Yu Rang Park","doi":"10.1093/braincomms/fcaf179","DOIUrl":"10.1093/braincomms/fcaf179","url":null,"abstract":"<p><p>Inflammatory diseases of the CNS impose a substantial disease burden, necessitating prompt and appropriate prognosis prediction. We developed a multimodal deep learning model integrating clinical features and brain MRI data to enhance early prognosis prediction of CNS inflammation. This retrospective study used thin-cut T1-weighted brain MRI scans and the clinical variables of patients with CNS inflammation who were admitted to a tertiary referral hospital between January 2010 and December 2023. Data collected after January 2022 served as the external test set. 3D MRI images were first segmented into 43 brain regions using the FastSurfer library. The segmented images were then processed through a 3D convolutional neural network model for feature extraction and vectorization, after which they were integrated with clinical features for prediction. The performance of each artificial intelligence model was assessed using accuracy, F1 score, area under the receiver operating characteristic curve and area under the precision-recall curve. The internal dataset comprised 413 images from 291 patients (mean age, 45.5 years ± 19.3 [SD]; 151 male patients; 54 with poor prognosis). The external dataset comprised 210 images from 106 patients (mean age, 45.5 years ± 18.9 [SD]; 59 male patients; 31 with poor prognosis). The multimodal deep learning model outperformed unimodal models across all aetiological groups, achieving area under the receiver operating characteristic curve values of 0.8048 for autoimmune, 0.9107 for bacterial, 1.0000 for tuberculosis and 0.9242 for viral infections. Furthermore, artificial intelligence assistance improved clinicians' prognostic accuracy, as demonstrated in comparisons with neurologists, paediatricians and radiologists. Our findings demonstrate that the multimodal deep learning model enhances artificial intelligence-assisted prognosis prediction in CNS inflammation, improving both model performance and clinician decision-making.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf179"},"PeriodicalIF":4.1,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12082089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096185","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":"Drug repurposing candidates for amyotrophic lateral sclerosis using common and rare genetic variants.","authors":"Zachary F Gerring, Oneil G Bhalala, Liam G Fearnley, Lotta E Oikari, Anthony R White, Eske M Derks, Rosie Watson, Nawaf Yassi, Melanie Bahlo, William R Reay","doi":"10.1093/braincomms/fcaf184","DOIUrl":"10.1093/braincomms/fcaf184","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative condition for which novel disease modifying therapies are urgently needed. Given the increasing bottlenecks in drug discovery pipelines, repurposing existing drugs for ALS may represent a path to expedite translation and improve disease outcomes. However, ALS is a heterogeneous disease for which the aetiology remains poorly characterized, complicating efforts to effectively repurpose drugs. We propose that the polygenic architecture of ALS genetic liability, which ranges from ultra-rare, high-impact variation to common frequency loci of small-individual effect, could be leveraged to prioritize drug repurposing candidates which are more generalizable to the ALS clinical population. Here, we utilize common and rare frequency ALS genetic risk with a novel approach to uncover therapeutic classes that may be prospective repurposing opportunities in ALS. The common variant-led analyses integrated both positional-based and functional gene-based tests on SNP-genotype data from a genome-wide association study of ALS and implicated mitogen-activated protein kinase signalling related downregulation through B-Raf inhibitors as a prospective target for repurposing. The rare variant-led approaches leveraged rare variant burden testing of exonic variation on whole genome-sequencing data from a subset of the common variant genome-wide association study cohort and prioritized B-vitamin related candidates, such as cobalamin and niacin. Clinical characterization of these putative repurposing opportunities revealed genetic support to existing biology for which related compounds are actively proceeding through ALS clinical studies. Moreover, leveraging transcriptomic data from ALS derived cell lines carrying a selection of pathogenic variants in genes that cause familial forms of ALS (<i>C9orf72</i>, <i>SOD1</i>, <i>FUS</i> and <i>TARDBP</i>) suggested that the action of B-Raf inhibitors may be of particular relevance to <i>C9orf72</i> carriers, whilst the signal for B-vitamin signalling related targets was strongest in <i>SOD1</i> carriers. In summary, we demonstrate the importance of considering the therapeutic actionability of both common and rare-variant mediated risk for ALS given the immense biological heterogeneity of this disorder. Future pre-clinical and clinical studies are now warranted to further characterize the tractability of these prioritized compounds.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf184"},"PeriodicalIF":4.1,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12089939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112777","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":"Two distinct trajectories of brain volume loss in myotonic dystrophy type 1 via machine learning.","authors":"Tomoki Imokawa, Hiroyuki Maki, Daichi Sone, Risa Kagaya, Yoko Shigemoto, Yukio Kimura, Hiroshi Matsuda, Yuji Takahashi, Ukihide Tateishi, Noriko Sato","doi":"10.1093/braincomms/fcaf181","DOIUrl":"10.1093/braincomms/fcaf181","url":null,"abstract":"<p><p>Myotonic dystrophy Type 1 is a disorder that affects multiple systems, including the muscles and the CNS. Previous studies have primarily used voxel-based morphometry to examine areas of brain volume reduction and their correlation with symptoms; however, consistent findings have not been obtained. Subtype and stage inference is an unsupervised machine learning algorithm that elucidates disease progression and subtypes from cross-sectional data. In this study, we used Subtype and Stage Inference to analyse the morphometric MRI data of patients with myotonic dystrophy Type 1 to reveal the detailed trajectories of brain volume loss and to explore the potential of morphometric MRI as a biomarker for myotonic dystrophy Type 1. We examined 60 patients with myotonic dystrophy Type 1 and 50 age- and sex-matched controls. The patients with myotonic dystrophy Type 1 had a median age of 44 years (range 20-67 years) and included 32 males. Using three-dimensional T1-weighted MRI images, we analysed the subtypes of brain involvement and their respective trajectories of brain volume loss with subtype and stage inference. Additionally, we examined the differences and correlations in clinical and brain morphological indicators between the identified subtypes and controls. Subtype and stage inference revealed two subtypes: cortical and subcortical. In the cortical subtype, volume reduction began in the precentral gyrus and spread primarily to the cerebral cortex. In the subcortical subtype, it progressed early in the putamen, thalamus, hippocampus and amygdala. Examination of clinical indicators showed that despite the younger age of the subcortical subtype compared to the cortical subtype, mini-mental state examination scores were significantly lower in the subcortical subtype and negatively correlated with subcortical probability. The total intracranial volume, a marker of maximal brain growth, was significantly smaller in the cortical subtype; however, it was not smaller in the subcortical subtype than in controls. Furthermore, the subcortical subtype showed a larger total ventricle volume than both the controls and the cortical subtype. In contrast, its total brain parenchymal volume was lower than that of the controls, similar to the cortical subtype. These results suggest early childhood brain development differences between the two subtypes. Using Subtype and Stage Inference, we identified two subtypes of myotonic dystrophy Type 1 and demonstrated the potential of morphological MRI as a biomarker for cognitive impairment and brain developmental disorders. Machine learning can aid in stratifying myotonic dystrophy Type 1 in clinical settings and contribute to the elucidation of its complex pathophysiology.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf181"},"PeriodicalIF":4.1,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144121650","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":"Physical activity and anodal-transcranial direct current stimulation: a synergistic approach to boost motor cortex plasticity.","authors":"Federica Marchiotto, Marco Cambiaghi, Mario Buffelli","doi":"10.1093/braincomms/fcaf167","DOIUrl":"https://doi.org/10.1093/braincomms/fcaf167","url":null,"abstract":"<p><p>The application of anodal-transcranial direct current stimulation (A-tDCS) over the primary motor cortex (M1) increases its structural and functional plasticity, as also physical exercise. Combining both interventions has a boosting effect, thus revealing a crucial role of the brain state during stimulation. Although brain slice and anesthetized animal studies support this, further investigation in awake animals is necessary. In the present study, we analyzed the effects of coupling A-tDCS with low-intensity physical activity on the mouse M1 structural and functional plasticity. C57BL/6 mice were monolaterally treated with M1 A-tDCS while walking on a rotarod or at rest. To assess the impact of our interventions, we analyzed both motor cortices for changes in neuronal activation, dendritic spine density, and functional synchronisation as measured by local field potential coherence. The combination of physical activity and M1 stimulation revealed a synergistic interhemispheric effect on cortical activation in both layers II/III and V, not present when using a single type of intervention. These data were accompanied by increased M1-M1 synchrony in the low-theta frequency, a hallmark of motor network activity in mice. Dendritic spine density revealed an effect of the combo, which was significantly higher only in layer II/III, accompanied by increased post-synaptic density protein 95 expression in the same area. Based on our findings, we propose that the efficacy of tDCS hinges on brain state rather than being merely a direct causal factor. The observed outcomes contribute to a deeper comprehension of the mechanisms governing structural and functional reorganisation within the motor cortex under physiological conditions, with potential implications for research on learning, memory, and neurological disorders such as stroke.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf167"},"PeriodicalIF":4.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12062577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144014388","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 troponin T reflects lower motor neuron involvement on electromyography in amyotrophic lateral sclerosis.","authors":"Sanharib Chamoun, Sofia Imrell, Zane Upate, Ulf Kläppe, Linn Öijerstedt, Solmaz Yazdani, Mikael Andersson Franko, Juliette Foucher, Louisa Azizi, Anikó Lovik, Kristin Samuelsson, Rayomand Press, Fang Fang, Emma Svennberg, Alexander Juto, Caroline Ingre","doi":"10.1093/braincomms/fcaf177","DOIUrl":"10.1093/braincomms/fcaf177","url":null,"abstract":"<p><p>Cardiac troponin T (cTnT) is elevated in neuromuscular conditions without apparent cardiac disease, including Amyotrophic Lateral Sclerosis (ALS). The reason for this increase is unclear. Since cTnT is found in both cardiomyocytes and skeletal muscle cells, we aimed to investigate the latter as a possible cTnT source. We examined the correlation of cTnT in venous blood to lower motor neuron (LMN) involvement on Electromyography (EMG). A positive correlation between EMG findings and cTnT levels would indicate that cTnT is a biomarker for LMN involvement in ALS. This observational cohort study was conducted on a tertiary referral centre for neuromuscular diseases in Stockholm, Sweden. Consecutive patients with ALS were included. EMG was performed during diagnostic work-up, and high-sensitive cardiac troponin T (hs-cTnT), plasma creatine kinase (CK), and serum neurofilament light (NfL) were analysed within 6 months of the EMG. King's stage and score on the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS-R) closest to hs-cTnT sampling were noted. In total, 50 ALS patients diagnosed between 1 January 2014 and 31 December 2018 were included and followed until death, invasive ventilation, or the 14 August 2024. Hs-cTnT correlated positively with the number of muscular regions involved (<i>τ</i> = 0.283, <i>P</i> = 0.009) and percentage of muscles involved on EMG (ρ = 0.367, <i>P</i> = 0.009). Hs-cTnT was associated with the percentage of muscles involved in EMG in the adjusted linear regression. Patients with higher hs-cTnT had more advanced King's stage, both when numerical hs-cTnT and subgrouping high (≥15 nanogram/L) versus normal hs-cTnT was used (τ = 0.253, <i>P</i> = 0.021 and <i>U</i> = 197.5, <i>P</i> = 0.022, respectively). Hs-cTnT was neither correlated to ALSFRS-R total score (ρ = -0.176, <i>P</i> = 0.220 and U = 249.5, <i>P</i> = 0.233, respectively) nor ALSFRS-R excluding respiratory domain score (<i>ρ</i> = -0.069, <i>P</i> = 0.632 and <i>U</i> = 280.5, <i>P</i> = 0.558, respectively). High versus normal hs-cTnT did not predict survival (univariate analysis, HR = 1.824, <i>P</i> = 0.060). Numerical hs-cTnT was associated with shorter survival (univariate analysis, HR = 1.635, <i>P</i> = 0.017) but not after adjusting for age at diagnosis (HR = 1.413, <i>P</i> = 0.105). This study illustrates that ALS patients with higher hs-cTnT have more spread disease as evidenced by the positive correlation between hs-cTnT and both EMG and King's stage. This is not true for established biomarkers of muscle damage (CK) and neuroaxonal damage (NfL). These findings need to be confirmed in larger studies but suggest that hs-cTnT is a biomarker of LMN involvement in patients with ALS and could be used in clinical trials.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf177"},"PeriodicalIF":4.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12082033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096256","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":"Post-stroke sensory hypersensitivity: insights from lesion-symptom and disconnection mapping.","authors":"Hella Thielen, Nora Tuts, Lies Welkenhuyzen, Robin Lemmens, Alain Wibail, Irene M C Huenges Wajer, Christophe Lafosse, Dante Mantini, Céline R Gillebert","doi":"10.1093/braincomms/fcaf176","DOIUrl":"10.1093/braincomms/fcaf176","url":null,"abstract":"<p><p>A post-injury increase in sensory sensitivity is frequently reported by acquired brain injury patients, including stroke patients. These symptoms are related to poor functional outcomes, but their underlying neural mechanisms remain unclear. Since stroke results in focal lesions that can easily be visualized on imaging, the lesions of stroke survivors can be used to study the neuroanatomy of post-injury sensory hypersensitivity. We used multivariate support vector regression lesion-symptom mapping and indirect structural disconnection mapping to uncover the lesion location and white matter tracts related to post-stroke sensory hypersensitivity. A total of 103 patients were included in the study, of which 47% reported post-stroke sensory hypersensitivity across different sensory modalities. The lesion-symptom and structural connectivity mapping identified the putamen, thalamus, amygdala and insula in the grey matter as well as fronto-insular tracts, and the fronto-striatal tract in the white matter as neural structures potentially involved in post-stroke sensory hypersensitivity. By examining the neuroanatomy of post-stroke sensory hypersensitivity in a large stroke sample, this study offers a significant advancement in our understanding of the neural basis of post-stroke sensory hypersensitivity.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf176"},"PeriodicalIF":4.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144096260","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":"Infratentorial white matter integrity as a potential biomarker for post-stroke aphasia.","authors":"Ben Zhang, Caroline Schnakers, Kevin Xing-Long Wang, Jing Wang, Sharon Lee, Henry Millan, Melissa Howard, Emily Rosario, Zhong Sheng Zheng","doi":"10.1093/braincomms/fcaf174","DOIUrl":"https://doi.org/10.1093/braincomms/fcaf174","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Traditionally, neuroimaging studies of post-stroke aphasia focus on supratentorial brain regions related to language function and recovery. However, stroke-induced lesions often distort these areas, posing a challenge for neuroimaging analyses aimed at identifying reliable biomarkers. This study seeks to explore alternative biomarkers in regions less affected by direct stroke damage, such as white matter regions below the tentorium, to overcome these methodological limitations. Diffusion tensor imaging was accomplished on 55 participants with chronic post-stroke aphasia. Focusing on regions below the tentorium, correlations were analysed between Western Aphasia Battery-Revised scores and average fractional anisotropy values. The volume of intersection between each participant's lesion and their left arcuate fasciculus was also analysed for correlations with Western Aphasia Battery-Revised scores as well. Linear regression analyses were then conducted using regions showing significant correlations as univariate predictors. After applying multiple comparisons corrections, we found that average fractional anisotropy in the middle cerebellar peduncle was positively correlated with aphasia quotient (&lt;i&gt;P&lt;/i&gt; = 0.004), spontaneous speech (&lt;i&gt;P&lt;/i&gt; = 0.005), auditory verbal comprehension (&lt;i&gt;P&lt;/i&gt; = 0.004), naming and word finding (&lt;i&gt;P&lt;/i&gt; = 0.005) and repetition (&lt;i&gt;P&lt;/i&gt; = 0.013). Average fractional anisotropy in the left inferior cerebellar peduncle positively correlated with spontaneous speech (&lt;i&gt;P&lt;/i&gt; = 0.018) and auditory verbal comprehension (&lt;i&gt;P&lt;/i&gt; = 0.018). Average fractional anisotropy in the left corticospinal tract positively correlated with aphasia quotient (&lt;i&gt;P&lt;/i&gt; = 0.019) and spontaneous speech (&lt;i&gt;P&lt;/i&gt; = 0.005). The volume of intersection between the left arcuate fasciculus and participant lesion was negatively correlated with aphasia quotient (&lt;i&gt;P&lt;/i&gt; = 0.014) and repetition (&lt;i&gt;P&lt;/i&gt; = 0.002). Through linear regression analyses, average fractional anisotropy of the middle cerebellar peduncle significantly predicted aphasia quotient and all subscores. Average fractional anisotropy of the left inferior cerebellar peduncle significantly predicted all scores except repetition. Average fractional anisotropy of the left corticospinal tract significantly predicted all scores except for auditory verbal comprehension. The volume of intersection between the left arcuate fasciculus and lesions significantly predicted all scores except for auditory verbal comprehension. These findings underscore the potential of infratentorial white matter regions as biomarkers of aphasia severity, encompassing overall and specific subdomain impairment. By shifting the focus to below the tentorium, it becomes possible to find more robust targets for further research and therapeutic interventions. This approach is not only able to sidestep analytical complications posed by cortical lesions, it also opens new doors for understanding complex cerebellar ","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf174"},"PeriodicalIF":4.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12079383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082758","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":"Cerebrovascular co-pathology and cholinergic white matter pathways along the Lewy body continuum.","authors":"Cene Jerele, Antonios Tzortzakakis, Milan Nemy, Anna Rennie, Javier Arranz, Victor Montal, Alexandre Bejanin, Dag Aarsland, Eric Westman, Juan Fortea, Alberto Lleó, Daniel Alcolea, Milica G Kramberger, Daniel Ferreira","doi":"10.1093/braincomms/fcaf173","DOIUrl":"10.1093/braincomms/fcaf173","url":null,"abstract":"<p><p>Dementia with Lewy bodies often presents with cholinergic degeneration and varying degrees of cerebrovascular disease. There is a lack of radiological methods for evaluating cholinergic degeneration in dementia with Lewy bodies. We investigated the potential of the Cholinergic Pathway Hyperintensities Scale (CHIPS) in identifying cerebrovascular disease-related disruptions in cholinergic white matter pathways, offering a practical and accessible method for assessing cholinergic integrity in neurodegenerative diseases. We assessed the associations of CHIPS with regional brain atrophy, Alzheimer's disease co-pathology and clinical phenotype. Additionally, we compared its diagnostic performance to that of other manual and automated evaluation methods. We included 82 individuals (41 patients in the Lewy body continuum with either probable dementia with Lewy bodies or mild cognitive impairment with Lewy bodies, and 41 healthy controls) from the Sant Pau Initiative on Neurodegeneration cohort. We used CHIPS to assess cholinergic white matter signal abnormalities (WMSA) on MRI, while tractography mean diffusivity provided a complementary measure of cholinergic WMSA. For global WMSA evaluation, we used the Fazekas scale and FreeSurfer. CHIPS successfully identified cerebrovascular disease-related disruptions in cholinergic white matter pathways, as evidenced by its association with tractography and global WMSA markers (<i>P</i> < 0.005 for all associations). Lewy body patients showed a significantly higher degree of WMSA in the external capsule cholinergic pathway despite no significant differences in global WMSA compared to controls. CHIPS score in the posterior external capsule and the mean diffusivity in the external capsule and cingulum exceeded the threshold for an optimal biomarker (sensitivity and specificity values above 80%) in discriminating Lewy body patients from controls. Furthermore, higher CHIPS scores, Fazekas scale and tractography mean diffusivity were associated with more pronounced frontal atrophy in Lewy body patients but not in controls. No associations were found for the four WMSA and integrity methods with the core clinical features, clinical or cognitive measures, or CSF biomarkers. In conclusion, cholinergic WMSA were more pronounced in Lewy body patients compared to healthy controls, independently of global WMSA. Our findings indicate that cerebrovascular disease-related disruptions in cholinergic white matter may be linked to frontal atrophy in Lewy body patients. Clinically, we demonstrate the potential of CHIPS to assess cholinergic WMSA using widely available MRI sequences. Our data suggest cerebrovascular disease co-pathology could drive the cholinergic degeneration in Lewy body patients, opening opportunities for therapeutic interventions targeting vascular health from mild cognitive impairment with Lewy bodies through manifest dementia with Lewy bodies.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf173"},"PeriodicalIF":4.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103290","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":"Differential modulation of neural oscillations in perception-action links in Tourette syndrome.","authors":"Astrid Prochnow, Annet Bluschke, Tina Rawish, Julia Friedrich, Yifan Hao, Christian Frings, Tobias Bäumer, Alexander Münchau, Christian Beste","doi":"10.1093/braincomms/fcaf172","DOIUrl":"10.1093/braincomms/fcaf172","url":null,"abstract":"<p><p>Gilles de la Tourette Syndrome (GTS) is a multi-faceted neuro-psychiatric disorder. While novel conceptions overcoming the criticized categorization of GTS as a movement disorder are on the rise, little is known about their neural implementation and whether there are links to known pathophysiological processes in GTS. This is the case for conceptions suggesting that aberrant perception-action processes reflect a key feature of GTS. Building on the concept that overly strong perception-action associations are pivotal to understanding GTS pathophysiology, we examined how these associations influence response inhibition and used EEG methods to examine the importance of theta, alpha and beta band activity due to their known relevance for GTS pathophysiology. In this case-control study, behavioural analyses revealed that adult patients with GTS experienced greater difficulty during motor response inhibition when perceptual features of Nogo stimuli overlapped with perceptual features of Go stimuli, indicating impaired reconfiguration of perception-action associations. Neurophysiological findings showed robust differential patterns of modulation in theta and alpha band activity between neurotypical (NT) individuals and GTS patients. Specifically, GTS patients exhibited stronger and more extended theta band modulation but weaker and more restricted alpha band modulation during overlapping Nogo trials than NT individuals. Unlike NT individuals, GTS patients did not exhibit beta band modulations necessary for dynamically handling perception-action codes. The findings highlight increased theta band modulation in GTS patients' significant stronger perception-action bindings and a lack of compensatory alpha band modulation. The robust differential modulation observed provides novel insights, emphasizing theta and alpha oscillations as key elements in GTS pathophysiology and offering potential implications for targeted cognitive-behavioural interventions.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf172"},"PeriodicalIF":4.1,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060835","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":"Sex differences in story recall decline in preclinical Alzheimer's disease.","authors":"Douglas Cowman, Rebecca Langhough, Hayley Olson, Kristin Basche, Leah Sanson-Miles, Davide Bruno, Bruce Hermann, Bradley T Christian, Tobey J Betthauser, Sterling C Johnson, Kimberly D Mueller","doi":"10.1093/braincomms/fcaf169","DOIUrl":"10.1093/braincomms/fcaf169","url":null,"abstract":"<p><p>Stage II pre-clinical Alzheimer's disease is defined by the presence of increased amyloid-beta evidenced by fluid and/or imaging biomarkers, in the absence of clinical signs and symptoms. Previous research suggests that pre-clinical sex differences exist on measures of story recall, such as the Wechsler memory scale-revised logical memory test total score. However, sex differences on a composite metric of proper names from that test have not been investigated, and the relationships between sex and amyloid positivity on longitudinal logical memory measures are unclear. We examined longitudinal trajectories of total score and proper names by sex (Aim 1), and by the combination of sex and amyloid status (Aim 2). <i>N</i> = 457 Wisconsin registry for Alzheimer's prevention participants with PET Pittsburgh compound B-assessed amyloid status (+/-) were included. Linear mixed-effects models were used to examine the interaction between sex and age at visit (the time variable), and sex and amyloid+/- on longitudinal total and proper name scores. Aim 1 analyses showed a main effect such that female participants, on average, scored higher than males on both total and proper name recall. The interaction between sex and age was not statistically significant, indicating that both sexes experienced a similar average rate of annual decline. Aim 2 analyses showed that amyloid positive participants, regardless of sex, showed steeper declines compared to amyloid negative, female participants (reference group). Thus, while female participants generally outperformed males on story recall measures, the impact of amyloid burden on longitudinal story recall trajectories was not significantly more pronounced in females. Results emphasize the need for further exploration into sex-specific cognitive reserve mechanisms in the context of Alzheimer's disease biomarker burden, as well as in the assessment and understanding of cognitive decline trajectories.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 3","pages":"fcaf169"},"PeriodicalIF":4.1,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103311","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}