ArticleAnnals of clinical and translational neurology2021
Selective vulnerability to atrophy in sporadic Creutzfeldt-Jakob disease.
Article in Annals of clinical and translational neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Neuropsychiatric symptoms in sporadic Creutzfeldt-Jakob disease.Brain : a journal of neurology · 2026Article
- Diagnosis and Management of Progressive Corticobasal Syndrome.Current treatment options in neurology · 2024Article
- Molecular and cellular mechanisms of selective vulnerability in neurodegenerative diseases.Nature reviews. Neuroscience · 2024Review
- PRNP expression predicts imaging findings in sporadic Creutzfeldt-Jakob disease.Annals of clinical and translational neurology · 2023Article
- Case report: Two clusters of Creutzfeldt-Jakob disease cases within 1 year in West Michigan.Frontiers in neurology · 2023Article
- Human prion diseases and the prion protein - what is the current state of knowledge?Translational neuroscience · 2023Review
- Default Mode Network quantitative diffusion and resting-state functional magnetic resonance imaging correlates in sporadic Creutzfeldt-Jakob disease.Human brain mapping · 2022Article
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Authors and funding
14 authors at 2 institutions in 3 countries.
Funding
Abstract
objectiveIdentification of brain regions susceptible to quantifiable atrophy in sporadic Creutzfeldt-Jakob disease (sCJD) should allow for improved understanding of disease pathophysiology and development of structural biomarkers that might be useful in future treatment trials. Although brain atrophy is not usually present by visual assessment of MRIs in sCJD, we assessed whether using voxel-based morphometry (VBM) can detect group-wise brain atrophy in sCJD.
methods3T brain MRI data were analyzed with VBM in 22 sCJD participants and 26 age-matched controls. Analyses included relationships of regional brain volumes with major clinical variables and dichotomization of the cohort according to expected disease duration based on prion molecular classification (i.e., short-duration/Fast-progressors (MM1, MV1, and VV2) vs. long-duration/Slow-progressors (MV2, VV1, and MM2)). Structural equation modeling (SEM) was used to assess network-level interactions of atrophy between specific brain regions.
resultssCJD showed selective atrophy in cortical and subcortical regions overlapping with all but one region of the default mode network (DMN) and the insulae, thalami, and right occipital lobe. SEM showed that the effective connectivity model fit in sCJD but not controls. The presence of visual hallucinations correlated with right fusiform, bilateral thalami, and medial orbitofrontal atrophy. Interestingly, brain atrophy was present in both Fast- and Slow-progressors. Worse cognition was associated with bilateral mesial frontal, insular, temporal pole, thalamus, and cerebellum atrophy.
interpretationBrain atrophy in sCJD preferentially affects specific cortical and subcortical regions, with an effective connectivity model showing strength and directionality between regions. Brain atrophy is present in Fast- and Slow-progressors, correlates with clinical findings, and is a potential biomarker in sCJD.
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