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.

Increased mammalian target of rapamycin signaling contributes to the accumulation of protein oxidative damage in a mouse model of down's syndrome / Tramutola, Antonella; Lanzillotta, Chiara; Arena, Andrea; Barone, Eugenio; Perluigi, Marzia; DI DOMENICO, Fabio. - In: NEURODEGENERATIVE DISEASES. - ISSN 1660-2854. - 16:1-2(2016), pp. 62-68. [10.1159/000441419]

Increased mammalian target of rapamycin signaling contributes to the accumulation of protein oxidative damage in a mouse model of down's syndrome

TRAMUTOLA, ANTONELLA;LANZILLOTTA, CHIARA;ARENA, ANDREA;BARONE, EUGENIO;PERLUIGI, Marzia;DI DOMENICO, FABIO
2016

Abstract

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.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11573/840612
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