한빛사논문
- 조회417
Kyu Hwan Shim 1, Danyeong Kim 1, Min Ju Kang 2, Jung-Min Pyun 3, Young Ho Park 4, Young Chul Youn 5, Kyung Won Park 6, Kyoungho Suk 7, Ho-Won Lee 8, Bárbara Fernandes Gomes 9, Henrik Zetterberg 9,10,11,12,13,14, Seong Soo A An 1, SangYun Kim 4; Alzheimer's Disease All Markers (ADAM) Research group
1Department of Bionano Technology, Gachon University, Seongnam, Republic of Korea.
2Department of Neurology, Veterans Medical Research Institute, Veterans Health Service Medical Center, Seoul, Republic of Korea.
3Department of Neurology, Soonchunhyang University Seoul Hospital, Soonchunhyang University College of Medicine, Seoul, Republic of Korea.
4Department of Neurology, Seoul National University College of Medicine and Clinical Neuroscience Center, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
5Department of Neurology, Chung-Ang University College of Medicine, Seoul, Republic of Korea.
6Department of Neurology, Dong-A University College of Medicine and Institute of Convergence Bio-Health, Busan, Republic of Korea.
7Department of Pharmacology, Kyungpook National University School of Medicine, Daegu, Republic of Korea.
8Department of Neurology, Kyungpook National University School of Medicine, Daegu, Republic of Korea.
9Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
10Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
11Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK.
12UK Dementia Research Institute at UCL, London, UK.
13Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China.
14Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Kyu Hwan Shim and Dan Yeong Kim contributed equally to this study.
CORRESPONDING AUTHORS : Seong Soo A. An, SangYun Kim
Abstract
Introduction: Alzheimer's disease (AD) involves the complement cascade, with complement component 3 (C3) playing a key role. However, the relationship between C3 and amyloid beta (Aβ) in blood is limited.
Methods: Plasma C3 and Aβ oligomerization tendency (AβOt) were measured in 35 AD patients and 62 healthy controls. Correlations with cerebrospinal fluid (CSF) biomarkers, cognitive impairment, and amyloid positron emission tomography (PET) were analyzed. Differences between biomarkers were compared in groups classified by concordances of biomarkers.
Results: Plasma C3 and AβOt were elevated in AD patients and in CSF or amyloid PET-positive groups. Weak positive correlation was found between C3 and AβOt, while both had strong negative correlations with CSF Aβ42 and cognitive performance. Abnormalities were observed for AβOt and CSF Aβ42 followed by C3 changes.
Discussion: Increased plasma C3 in AD are associated with amyloid pathology, possibly reflecting a defense response for Aβ clearance. Further studies on Aβ-binding proteins will enhance understanding of Aβ mechanisms in blood.
논문정보
- Research article
- 2024년 02월 (BRIC 등록일 2024-02-29)
- 국내(교신)+국외 연구진
- 의약학 > 신경의학
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