Traumatic brain injury (TBI) triggers progressive neurodegeneration resulting in brain atrophy that continues months-to-years following injury. However, a comprehensive characterization of the spatial and temporal evolution of TBI-related brain atrophy remains incomplete. Utilizing a sensitive and unbiased morphometry analysis pipeline optimized for detecting longitudinal changes, we analyzed a sample consisting of 37 individuals with moderate-severe TBI who had primarily high-velocity and high-impact injury mechanisms. They were scanned up to three times during the first year after injury (3 months, 6 months, and 12 months post-injury) and compared with 33 demographically matched controls who were scanned once. Individuals with TBI already showed cortical thinning in frontal and temporal regions and reduced volume in the bilateral thalami at 3 months post-injury. Longitudinally, only a subset of cortical regions in the parietal and occipital lobes showed continued atrophy from 3 to 12 months post-injury. Additionally, cortical white matter volume and nearly all deep gray matter structures exhibited progressive atrophy over this period. Finally, we found that disproportionate atrophy of cortex along sulci relative to gyri, an emerging morphometric marker of chronic TBI, was present as early as 3 month post-injury. In parallel, neurocognitive functioning largely recovered during this period despite this pervasive atrophy. Our findings demonstrate msTBI results in characteristic progressive neurodegeneration patterns that are divergent across regions and scale with the severity of injury. Future clinical research using atrophy during the first year of TBI as a biomarker of neurodegeneration should consider the spatiotemporal profile of atrophy described in this study.
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http://dx.doi.org/10.1002/hbm.26410 | DOI Listing |
Neurology
January 2025
Department of Neurology, Clinical Neuroscience Center, University Hospital and University of Zurich, Zurich, Switzerland.
Background And Objectives: Mesial temporal lobe epilepsy (mTLE) is generally associated with focal brain atrophy, but little knowledge exists on possible disease-related hypertrophy of brain structures. We hypothesized that repeated seizures or adaptive plasticity may lead to focal brain hypertrophy and aimed to investigate associated clinical correlates.
Methods: In this cohort study, we included patients with mTLE undergoing detailed epilepsy evaluations and matched healthy volunteers (HVs) from 2 tertiary centers (discovery and validation cohorts).
Neurol Neuroimmunol Neuroinflamm
January 2025
From the Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin Ultrahigh Field Facility (B.U.F.F.); Experimental and Clinical Research Center, Charité - Universitätsmedizin Berlin, Germany; Division of Paediatric Neurology, Department of Paediatrics I, Medical University of Innsbruck, Austria; Department of Pediatric Neurology, Olgahospital/Klinikum Stuttgart; Department of Paediatric Neurology, Children's Hospital Datteln, Witten/Herdecke University and Department of Neurology, Charité - Universitätsmedizin Berlin, Germany.
Background And Objectives: Pediatric patients with acute disseminated encephalomyelitis (ADEM) are at risk of impaired brain growth, with long-term neuropsychiatric consequences. We previously reported transient expansions of cerebral ventricle volume (VV) in experimental autoimmune encephalomyelitis, which subsequently normalized. In this study, we investigated changes in VV in ADEM in relation to other brain structures and clinical outcomes.
View Article and Find Full Text PDFClin J Am Soc Nephrol
December 2024
Department of Biomedical engineering, Emory University, Atlanta, GA, USA.
Background: Interstitial fibrosis and tubular atrophy (IFTA), and density and shape of peritubular capillaries (PTCs), are independently prognostic of disease progression. This study aimed to identify novel digital biomarkers of disease progression and assess the clinical relevance of the interplay between a variety of PTC characteristics and their microenvironment in glomerular diseases.
Methods: A total of 344 NEPTUNE/CureGN participants were included: 112 minimal change disease, 134 focal segmental glomerulosclerosis, 61 membranous nephropathy, and 37 IgA nephropathy.
Retina
November 2024
Ophthalmology Department, Hospital Lariboisiere and Fernand-Widal, Paris, France.
Cereb Cortex
December 2024
Rockefeller Neuroscience Institute 33 Medical Center Dr. Morgantown, WV 26505, United States.
Early-onset Alzheimer's disease (EOAD) is less investigated than the more common late-onset Alzheimer's disease (LOAD) despite its more aggressive course. A cortical signature of EOAD was recently proposed and may facilitate EOAD investigation. Here, we aimed to validate this proposed MRI biomarker of EOAD neurodegeneration in an Appalachian clinical cohort.
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