Hyemin Jang1,2, Hee Jin Kim1,2, Seongbeom Park1,2, Yu Hyun Park1,2, Yeongsim Choe1,2, Hanna Cho3, Chul Hyoung Lyoo3, Uicheul Yoon4, Jin San Lee5, Yeshin Kim6, Seung Joo Kim1,2, Jun Pyo Kim1,2, Young Hee Jung1,2, Young Hoon Ryu7, Jae Yong Choi8, Seung Hwan Moon9, Joon-Kyung Seong10, Charles DeCarli11, Michael W Weiner12, Samuel N Lockhart13, Soo Hyun Cho14, Duk L Na1,2,15,16, Sang Won Seo17,18,19,20,21. 1. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Gangnam-gu, Seoul, 135-710, South Korea. 2. Neuroscience Center, Samsung Medical Center, Seoul, South Korea. 3. Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 4. Department of Biomedical Engineering, College of Health and Medical Science, Catholic University of Daegu, Gyeongsan, South Korea. 5. Department of Neurology, Kyung Hee University Hospital, Seoul, South Korea. 6. Department of Neurology, Kangwon National University Hospital, Kangwon National University College of Medicine, Chuncheon, South Korea. 7. Department of Nuclear Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 8. Division of RI-Convergence Research, Korea Institute Radiological and Medical Sciences, Seoul, South Korea. 9. Departments of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. 10. School of Biomedical Engineering, Korea University, Seoul, South Korea. 11. Department of Neurology and Center for Neuroscience, University of California, Davis, Davis, USA. 12. Center for Imaging of Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, USA. 13. Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA. 14. Department of Neurology, Chonnam National University Hospital, Gwangju, South Korea. 15. Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea. 16. Samsung Alzheimer Research Center, Samsung Medical Center, Seoul, South Korea. 17. Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Gangnam-gu, Seoul, 135-710, South Korea. sangwonseo@empal.com. 18. Neuroscience Center, Samsung Medical Center, Seoul, South Korea. sangwonseo@empal.com. 19. Samsung Alzheimer Research Center, Samsung Medical Center, Seoul, South Korea. sangwonseo@empal.com. 20. Department of Clinical Research Design and Evaluation, SAIHST, Sungkyunkwan University, Seoul, South Korea. sangwonseo@empal.com. 21. Center for Clinical Epidemiology, Samsung Medical Center, Seoul, South Korea. sangwonseo@empal.com.
Abstract
OBJECTIVE: To apply an AT (Aβ/tau) classification system to subcortical vascular cognitive impairment (SVCI) patients following recently developed biomarker-based criteria of Alzheimer's disease (AD), and to investigate its clinical significance. METHODS: We recruited 60 SVCI patients who underwent the neuropsychological tests, brain MRI, and 18F-florbetaben and 18F-AV1451 PET at baseline. As a control group, we further recruited 27 patients with AD cognitive impairment (ADCI; eight Aβ PET-positive AD dementia and 19 amnestic mild cognitive impairment). ADCI and SVCI patients were classified as having normal or abnormal Aβ (A-/A+) and tau (T-/T+) based on PET results. Across the three SVCI groups (A-, A+T-, and A+T+SVCI), we compared longitudinal changes in cognition, hippocampal volume (HV), and cortical thickness using linear mixed models. RESULTS: Among SVCI patients, 33 (55%), 20 (33.3%), and seven (11.7%) patients were A-, A+T-, and A+T+, respectively. The frequency of T+ was lower in A+SVCI (7/27, 25.9%) than in A+ADCI (14/20, 70.0%, p = 0.003) which suggested that cerebral small vessel disease affected cognitive impairments independently of A+. A+T-SVCI had steeper cognitive decline than A-SVCI. A+T+SVCI also showed steeper cognitive decline than A+T-SVCI. Also, A+T-SVCI had steeper decrease in HV than A-SVCI, while cortical thinning did not differ between the two groups. A+T+SVCI had greater global cortical thinning compared with A+T-SVCI, while declines in HV did not differ between the two groups. CONCLUSION: This study showed that the AT system successfully characterized SVCI patients, suggesting that the AT system may be usefully applied in a research framework for clinically diagnosed SVCI.
OBJECTIVE: To apply an AT (Aβ/tau) classification system to subcortical vascular cognitive impairment (SVCI)patients following recently developed biomarker-based criteria of Alzheimer's disease (AD), and to investigate its clinical significance. METHODS: We recruited 60 SVCI patients who underwent the neuropsychological tests, brain MRI, and 18F-florbetaben and 18F-AV1451 PET at baseline. As a control group, we further recruited 27 patients with AD cognitive impairment (ADCI; eight Aβ PET-positive AD dementia and 19 amnestic mild cognitive impairment). ADCI and SVCI patients were classified as having normal or abnormal Aβ (A-/A+) and tau (T-/T+) based on PET results. Across the three SVCI groups (A-, A+T-, and A+T+SVCI), we compared longitudinal changes in cognition, hippocampal volume (HV), and cortical thickness using linear mixed models. RESULTS: Among SVCI patients, 33 (55%), 20 (33.3%), and seven (11.7%) patients were A-, A+T-, and A+T+, respectively. The frequency of T+ was lower in A+SVCI (7/27, 25.9%) than in A+ADCI (14/20, 70.0%, p = 0.003) which suggested that cerebral small vessel disease affected cognitive impairments independently of A+. A+T-SVCI had steeper cognitive decline than A-SVCI. A+T+SVCI also showed steeper cognitive decline than A+T-SVCI. Also, A+T-SVCI had steeper decrease in HV than A-SVCI, while cortical thinning did not differ between the two groups. A+T+SVCI had greater global cortical thinning compared with A+T-SVCI, while declines in HV did not differ between the two groups. CONCLUSION: This study showed that the AT system successfully characterized SVCI patients, suggesting that the AT system may be usefully applied in a research framework for clinically diagnosed SVCI.
Entities:
Keywords:
Amyloid-β; Classification; Longitudinal changes; Subcortical vascular cognitive impairment; Tau
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