Elevated Cerebrospinal Fluid and Plasma N-Cadherin in Alzheimer Disease. Issue 5 (7th March 2020)

• Record Type: Journal Article
• 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
• Is Part Of: Journal of neuropathology and experimental neurology. Volume 79:Issue 5(2020)
• Page Start: 484
• Page End: 492
• Publication Date: 2020-03-07
• Subjects: Alzheimer disease -- Brain -- Cerebrospinal fluid -- Dementia -- N-cadherin; Neurology -- Diseases -- Periodicals; Neurology -- Diseases -- Physiopathology -- Periodicals; 616.8047
• DOI: 10.1093/jnen/nlaa019
• Languages: English
• ISSNs: 0022-3069

Abstract

Abstract: N-cadherin is a synaptic adhesion molecule stabilizing synaptic cell structure and function. Cleavage of N-cadherin by γ-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.