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Original Paper

Increased Mammalian Target of Rapamycin Signaling Contributes to the Accumulation of Protein Oxidative Damage in a Mouse Model of Down's Syndrome

Tramutola A.a · Lanzillotta C.a · Arena A.a · Barone E.a, b · Perluigi M.a · Di Domenico F.a

Author affiliations

aDepartment of Biochemical Sciences, Sapienza University of Rome, Rome, Italy; bInstituto de Ciencias Biomédicas, Facultad de Salud, Universidad Autónoma de Chile, Santiago, Chile

Related Articles for ""

Neurodegener Dis 2016;16:62-68

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: June 01, 2015
Accepted: October 01, 2015
Published online: November 26, 2015
Issue release date: February 2016

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 1

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD

Abstract

Background: Neurodegenerative diseases are characterized by increased levels of oxidative stress and an altered mammalian target of rapamycin (mTOR)/autophagy axis; however, the mutual relationship between these two events is controversial. Previous studies in Down's syndrome (DS) and Alzheimer's disease (AD) suggested that the accumulation of protein oxidative damage results from the increased free radical production, mainly related to metabolic alterations, mitochondrial degeneration and amyloid-β deposition, and aberrant activity of protein degradative systems. Summary: This study analyzed mTOR signaling in Ts65Dn mice, a model of DS, at 6 and 12 months of age compared with euploid mice showing the early aberrant hyperphosphorylation of mTOR coupled with the reduction of autophagosome formation. Moreover, the evaluation of protein oxidation shows an increase in protein nitration and protein-bound 4-hydroxynonenal in 12-month-old Ts65Dn mice suggesting the potential involvement of altered autophagy in the buildup of protein oxidative damage. In addition, data obtained on cell culture support the protective role of autophagy in reducing protein oxidation. Key Messages: Overall, this study provides further evidence for the role of mTOR hyperactivation and reduced autophagy in the accumulation of protein oxidative damage during DS and AD pathologies.

© 2015 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: June 01, 2015
Accepted: October 01, 2015
Published online: November 26, 2015
Issue release date: February 2016

Number of Print Pages: 7
Number of Figures: 2
Number of Tables: 1

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


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