서상원 교수

These results indicate that cerebral MB is one of the important factors that cause cognitive impairments in SVaD.

Our findings suggest that although deep CMBs are mainly linked to subcortical SVD, both subcortical SVD and amyloid-related pathologies (eg, CAA) contribute to the pathogenesis of lobar CMBs, at least in subjects with mixed lobar and deep CMBs. Furthermore, subcortical SVD and amyloid-related pathologies interact to increase the risk of lobar CMBs.

Brain age estimation from anatomical features has been attracting more attention in recent years. This interest in brain age estimation is motivated by the importance of biological age prediction in health informatics, with an application to early prediction of neurocognitive disorders. It is well-known that normal brain aging follows a specific pattern, which enables researchers and practitioners to predict the age of a human's brain from its degeneration. In this paper, we model brain age pred

Our study suggested that svMCI was distinct from aMCI in terms of neuropsychological and PET findings, which may explain their clinical manifestations.

Our findings suggest that patients with CVD in the absence of Alzheimer's disease pathology can be demented, showing cognitive impairment in multiple domains, which is consistent with the topography of cortical thinning and hippocampal shape deformity.

Our results suggest that the impacts of AD and CVD pathologies on cognition are mediated by specific brain regions.

Imaging-pathological correlation studies show that <i>in vivo</i> amyloid-β (Aβ) positron emission tomography (PET) strongly predicts the presence of significant Aβ pathology at autopsy. We sought to determine whether regional PiB-PET uptake would improve sensitivity for amyloid detection in comparison with global measures (experiment 1), and to estimate the relative contributions of different Aβ aggregates to <i>in vivo</i> PET signal (experiment 2). In experiment 1, 54 subjects with [<sup>11</