Elevated Cerebrospinal Fluid and Plasma N-Cadherin in Alzheimer Disease
- Authors
- Choi, Ji-Young; Cho, Sun-Jung; Park, Jung Hyun; Yun, Sang-Moon; Jo, Chulman; Kim, Eun-Joo; Huh, Gi Yeong; Park, Moon Ho; Han, Changsu; Koh, Young Ho
- Issue Date
- 5월-2020
- Publisher
- OXFORD UNIV PRESS INC
- Keywords
- Alzheimer disease; Brain; Cerebrospinal fluid; Dementia; N-cadherin
- Citation
- JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, v.79, no.5, pp.484 - 492
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
- Volume
- 79
- Number
- 5
- Start Page
- 484
- End Page
- 492
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/56178
- DOI
- 10.1093/jnen/nlaa019
- ISSN
- 0022-3069
- Abstract
- N-cadherin is a synaptic adhesion molecule stabilizing synaptic cell structure and function. Cleavage of N-cadherin by gamma-secretase produces a C-terminal fragment, which is increased in the brains of Alzheimer disease (AD) patients. Here, we investigated the relationship between fluid N-cadherin levels and AD pathology. We first showed that the cleaved levels of N-cadherin were increased in homogenates of postmortem brain from AD patients compared with that in non-AD patients. We found that cleaved N-cadherin levels in the cerebrospinal fluid were increased in AD dementia compared with that in healthy control. ELISA results revealed that plasma levels of N-cadherin in 76 patients with AD were higher than those in 133 healthy control subjects. The N-cadherin levels in the brains of an AD mouse model, APP Swedish/PS1delE9 Tg (APP Tg) were reduced compared with that in control. The N-terminal fragment of N-cadherin produced by cleavage at a plasma membrane was detected extravascularly, accumulated in senile plaques in the cortex of an APP Tg mouse. In addition, N-cadherin plasma levels were increased in APP Tg mice. Collectively, our study suggests that alteration of N-cadherin levels might be associated with AD pathology.
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