Joonho Kim1, Han Kyu Na1, Jeong-Hyeon Shin1, Hee Jin Kim1, Sang Won Seo1, Joon-Kyung Seong2, Duk L Na2. 1. From the Department of Neurology, Severance Hospital (H.K.N.), Yonsei University College of Medicine (J.K.), Seoul; Department of Bio-convergence Engineering (J.-H.S., J.-K.S.), and School of Biomedical Engineering (J.-K.S.), Korea University, Seoul; and Department of Neurology, Sungkyunkwan University School of Medicine (H.J.K., S.W.S., D.L.N.), and Neuroscience Center (H.J.K., S.W.S., D.L.N), Samsung Medical Center, Seoul, Republic of Korea. 2. From the Department of Neurology, Severance Hospital (H.K.N.), Yonsei University College of Medicine (J.K.), Seoul; Department of Bio-convergence Engineering (J.-H.S., J.-K.S.), and School of Biomedical Engineering (J.-K.S.), Korea University, Seoul; and Department of Neurology, Sungkyunkwan University School of Medicine (H.J.K., S.W.S., D.L.N.), and Neuroscience Center (H.J.K., S.W.S., D.L.N), Samsung Medical Center, Seoul, Republic of Korea. dukna@skku.edu jkseong@korea.ac.kr.
Abstract
OBJECTIVE: To investigate differential atrophy patterns based on the presence of cortical superficial siderosis (cSS) and the role of cSS in predicting amyloid positivity in memory clinic patients fulfilling the diagnostic criteria for probable cerebral amyloid angiopathy (CAA). METHODS: We retrospectively collected data from 44 cognitively impaired patients with probable CAA who underwent 3-dimensional, T1-weighted MRIs (cSS+, n = 27; cSS-, n = 17). Amyloid-positive patients with Alzheimer disease (AD) (n = 56) and amyloid-negative cognitively normal participants (n = 34) were recruited as controls. Among the patients with CAA who underwent amyloid-PET scans (75.0%), we investigated whether amyloid-negative cases were unevenly distributed based on cSS presentation. APOE genotypes, Mini-Mental State Examination scores, and cortical atrophy pattern along with hippocampal volume were compared across groups. RESULTS: Ten patients with probable CAA presented amyloid negativity and all of them belonged to the cSS- group (58.8%). Compared to the cSS- group, the cSS+ group presented higher APOE ε4 frequency, worse memory dysfunction, and lower hippocampal volume. Compared with cognitively normal participants, the cSS+ group exhibited atrophy in the precuneus, posterior cingulate, parietotemporal, superior frontal, and medial temporal areas, a pattern similar to AD-specific atrophy. The cSS- group exhibited atrophy in the parietotemporal, superior frontal, and precentral regions. CONCLUSION: Our findings imply that the current version of the Boston criteria may not be sufficient enough to remove non-CAA cases from a cognitively impaired population, especially in the absence of cSS. Patients with probable CAA presenting cSS appear to reflect a CAA phenotype that shares pathologic hallmarks with AD, providing insight into the CAA-to-AD continuum.
OBJECTIVE: To investigate differential atrophy patterns based on the presence of cortical superficial siderosis (cSS) and the role of cSS in predicting amyloid positivity in memory clinic patients fulfilling the diagnostic criteria for probable cerebral amyloid angiopathy (CAA). METHODS: We retrospectively collected data from 44 cognitively impairedpatients with probable CAA who underwent 3-dimensional, T1-weighted MRIs (cSS+, n = 27; cSS-, n = 17). Amyloid-positive patients with Alzheimer disease (AD) (n = 56) and amyloid-negative cognitively normal participants (n = 34) were recruited as controls. Among the patients with CAA who underwent amyloid-PET scans (75.0%), we investigated whether amyloid-negative cases were unevenly distributed based on cSS presentation. APOE genotypes, Mini-Mental State Examination scores, and cortical atrophy pattern along with hippocampal volume were compared across groups. RESULTS: Ten patients with probable CAA presented amyloid negativity and all of them belonged to the cSS- group (58.8%). Compared to the cSS- group, the cSS+ group presented higher APOE ε4 frequency, worse memory dysfunction, and lower hippocampal volume. Compared with cognitively normal participants, the cSS+ group exhibited atrophy in the precuneus, posterior cingulate, parietotemporal, superior frontal, and medial temporal areas, a pattern similar to AD-specific atrophy. The cSS- group exhibited atrophy in the parietotemporal, superior frontal, and precentral regions. CONCLUSION: Our findings imply that the current version of the Boston criteria may not be sufficient enough to remove non-CAA cases from a cognitively impaired population, especially in the absence of cSS. Patients with probable CAA presenting cSS appear to reflect a CAA phenotype that shares pathologic hallmarks with AD, providing insight into the CAA-to-AD continuum.
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