Clinical relevance of plasma ADAM-17 with cognition and neurodegeneration in Alzheimer's disease.

IF 3.4 3区 医学 Q2 NEUROSCIENCES Journal of Alzheimer's Disease Pub Date : 2025-02-16 DOI:10.1177/13872877251317659
Zu-Qi Chen, Meng-Ting Wang, Cheng-Rong Tan, Shan Huang, Fa-Ying Zhou, Ying-Ying Shen, Gui-Hua Zeng, Dong-Yu Fan, Yan-Jiang Wang
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引用次数: 0

Abstract

Background: A disintegrin and metalloproteinase 17 (ADAM-17) has multiple pathophysiological functions in Alzheimer's disease (AD). However, the clinical relevance of ADAM-17 in AD is not clear yet.

Objective: This study aims to investigate the levels of circulating ADAM-17 and their association with AD.

Methods: This cross-sectional study recruited 40 normal cognition (NC) participants and 36 AD patients. Plasma ADAM-17 and biomarkers of neurodegeneration were determined. The association of plasma ADAM-17 with cognitive functions and biomarkers of neurodegeneration was analyzed.

Results: Plasma ADAM-17 levels were elevated in AD patients in comparison with NC subjects. Plasma ADAM-17 was positively associated with Clinical Dementia Rating (CDR) scores, but negatively associated with the Mini-Mental State Examination scores and Montreal Cognitive Assessment scores. Plasma ADAM-17 levels were positively associated with the levels of Aβ40, Aβ42, and p-Tau181.

Conclusions: These findings suggest a link between ADAM-17 and the pathogenesis of AD from a clinical perspective.

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来源期刊
Journal of Alzheimer's Disease
Journal of Alzheimer's Disease 医学-神经科学
CiteScore
6.40
自引率
7.50%
发文量
1327
审稿时长
2 months
期刊介绍: The Journal of Alzheimer''s Disease (JAD) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer''s disease. The journal publishes research reports, reviews, short communications, hypotheses, ethics reviews, book reviews, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer''s disease.
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