Significant Upregulation of Alzheimer's β‐Amyloid Levels in a Living System Induced by Extracellular Elastin Polypeptides. (4th November 2019)

• Record Type: Journal Article
• Authors: Ma, Chao; Su, Juanjuan; Sun, Yao; Feng, Yang; Shen, Nolan; Li, Bo; Liang, Yingxia; Yang, Xintong; Wu, Hui; Zhang, Hongjie; Herrmann, Andreas; Tanzi, Rudolph E.; Liu, Kai; Zhang, Can
• Is Part Of: Angewandte Chemie. Volume 131:Number 51(2019)
• Page Start: 18876
• Page End: 18882
• Publication Date: 2019-11-04
• Subjects: Alzheimer -- Amyloid-β-Peptide -- Extrazelluläres Elastin -- Hochregulierung; Chemistry -- Periodicals; 540
• DOI: 10.1002/ange.201912399
• Languages: English
• ISSNs: 0044-8249

Abstract

Abstract: Alzheimer's disease (AD) is a neurodegenerative disorder and the primary cause of age‐related dementia. The etiology of AD is complex and has not been completely elucidated. Herein, we report that treatment with elastin‐like polypeptides (ELPs), a component of the brain extracellular matrix (ECM), significantly increased the levels of AD‐related amyloid‐β peptides (Aβ) both in vitro and in vivo. Regarding the molecular mechanism(s), the upregulation of Aβ levels was related to increased proteolytic processing of the amyloid precursor protein. Furthermore, nesting tests demonstrated that the ELP‐treated animals showed significant neurobehavioral deficits with cognitive impairment. These results suggest that the elastin is associated with AD‐related pathological and behavioral changes. This finding presents a new aspect for Alzheimer's amyloidosis event and provides a great promise in developing ELP‐based model systems to better understand the pathogenesis of AD. Abstract : Die Behandlung mit Elastin‐Polypeptiden, einer Komponente der extrazellulären Matrix (ECM) des Gehirns, erhöht die Konzentration von β‐Amyloid, das mit Alzheimer in Verbindung gebracht wird, sowohl in vitro als auch in vivo. Bei Tieren steht das Auftreten von kognitiven Beeinträchtigungen im Anfangsstadium hiermit in Zusammenhang. Die Behandlung liefert neue Einblicke in die Pathogenese der Alzheimer‐Erkrankung.