BackgroundMild traumatic brain injury (mTBI) in former contact sports athletes is a risk factor for dementia. However, it is unknown why only some individuals with mTBI develop dementia, suggesting that head injury exposure alone is not sufficient to produce the condition. We hypothesize that mTBI could be associated with neurodegenerative processes that target specific brain structures and connectivity networks and increase vulnerability to dementia.Method46 male former professional athletes with a history of multiple concussions were recruited. To compare participants with evidence of underlying pathology versus participants without any evidence, the sample was divided into neurodegenerative biomarker positive (N+, n = 25) and negative (N‐, n = 21) groups. The division was based on the positivity in at least one of these biomarkers: cerebrospinal fluid total tau (> 300 pg/ml), cortical positron emission tomography tau standardized uptake value ratio (>1.30) and serum neurofilament light‐chain (> 12.5 pg/ml). Groups were matched for age and number of concussions. Cognitive profiles were assessed by comparing the following scores between groups: Trail Making Test ratio, Digit Span Backwards, Paced Auditory Serial Addition Test, verbal fluency, and Rey Auditory Verbal Learning Test (RAVLT). Grey matter volume was calculated by voxel‐based morphometry and compared between groups. Functional connectivity differences were evaluated for the default mode (DMN), the salience (SN) and the dorsal attention (DAN) networks.Results(N+) presented more number of intrusions at immediate (p = 0.04, FDR corrected) and short delay recall (p = 0.02, FDR corrected) and worse recognition discrimination index (p = 0.02, FDR corrected) in the RAVLT in comparison to (N‐). In addition, (N+) displayed more atrophy in the left frontal superior and middle gyrus (p < 0.001, extended threshold = 50 voxels) and disconnection of the DAN (p < 0.001, FWE cluster correction) versus (N‐). No significant differences were obtained for the DMN and SN.ConclusionFrontal atrophy and DAN abnormal connectivity may underlie cognitive deficits in the (N+) group. Biomarkers of neurodegeneration provide a sensitive tool to detect participants with structural and functional changes and may associate with higher risk to develop dementia after mTBI.
Background Corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP) are two syndromes associated with frontotemporal lobar degeneration (FTLD) with heterogeneous presentation and progression. Co‐pathology of FTLD and Alzheimer’s disease (AD) has been described and could influence the clinical presentation of CBS and PSP. The goal of this study is to evaluate the role of AD pathology in CBS and PSP, by analyzing functional and structural neuroimaging and memory performance. Method Patients with a clinical diagnosis of PSP and CBS (n=15) and AD (n=18) underwent functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (DTI). Patients were separated according to AD biomarker positivity (CBS‐PSP‐AD, n=6) and negativity (CBS‐PSP‐noAD, n=9) based on the presence of AD biomarkers in cerebrospinal fluid. FMRI images were preprocessed to assess connectivity differences in the default mode network (DMN). DTI was analyzed to trace the bilateral superior longitudinal fasciculus (SLF) and extract its fractional anisotropy and mean diffusivity. Verbal learning and memory were assessed with the California Verbal Learning Test (CVLT‐II) and the Consortium to Establish a Registry for Alzheimer’s disease (CERAD) of the Toronto Cognitive Assessment, and the z‐scores were compared between groups. Result The DMN showed reduced functional connectivity in the groups with AD biomarker positivity (CBS‐PSP‐AD and AD patients) relative to the CBS‐PSP‐noAD group. Specifically, reduced connectivity was observed between the left angular gyrus and the left (T(23) = ‐4.02, p‐FDR= 0.02) and right (T(23) = ‐3.48, p‐FDR=0.04) lateral parietal regions in AD vs CBS‐PSP‐noAD. Reduced connectivity was found between the left angular gyrus, the posterior cingulate cortex (T(11) = ‐4.72, p‐FDR=0.02) and the right hippocampus (T(11) = ‐3.94, p‐FDR=0.04) in CBS‐PSP‐AD vs CBS‐PSP‐noAD. No differences were found in DMN connectivity in AD vs CBS‐PSP‐AD. SLF tractography metrics showed no difference between groups. Both CBS‐PSP‐AD and AD patients had significantly worse delayed memory scores than the CBS‐PSP‐noAD group (post‐hoc p‐FDR=0.01). Conclusion There are similarities between AD positive biomarker groups (CBS‐PSP‐AD and AD patients) in functional connectivity and memory scores, with these groups differing from the CBS‐PSP‐noAD patients. These results suggest that pathology can mediate functional connectivity patterns and influence clinical manifestation.
Background The capacity to ascertain other people’s emotional states is crucial for establishing and maintaining social interactions. In particular, accurate recognition of facial expressions and beliefs about whether we trust what a face transmits are fundamental for guiding and adjusting this social behavior. Yet, although emotion recognition impairments are well documented in neurodegenerative diseases, the role of monitoring skills in this domain remains poorly understood in the field of dementia. Method We recruited patients with behavioral variant frontotemporal dementia (bvFTD, n = 18), Alzheimer’s disease (AD, n = 27), and demographically‐matched controls (n = 38). Participants performed a classic test of facial expression recognition and, after each trial, they provided a confidence judgment about their performance. A monitoring index was calculated considering both performance on each emotion type and associated confidence ratings (with higher values of the index indicating worse monitoring). Then, whole‐brain grey matter volume was analyzed via voxel‐based morphometry (VBM) to track possible associations with the monitoring index. Results Compared to controls, both groups of patients exhibited difficulties in monitoring negative emotions. Monitoring of disgust was specifically impaired in bvFTD, and monitoring of sadness and neutral faces, in AD. VBM results showed that, in bvFTD, reduced grey matter volume in areas belonging to the limbic system and subcortical regions was associated with emotion recognition deficits. Monitoring impairments were also related with different subcortical and cortical areas, including the prefrontal lobe, insula and the cingulate cortex. On the other hand, in AD, temporal and parietal areas were associated with emotion recognition and parietal and frontal regions, with monitoring. Conclusion These results indicate that dementia patients present emotion recognition monitoring impairments and that these deficits are associated with damage of cortical and subcortical regions as well as limbic circuits. In both groups, recognition and monitoring of emotions shared several structural substrates. The monitoring impairments presented in bvFTD and AD could be related with the changes in social cognition and behavior that these patients presented in daily life. Therefore, these preliminary findings could contribute to a better understanding of emotion monitoring processes.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.