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Elena Tamagno

Researcher at University of Turin

Publications -  70
Citations -  9612

Elena Tamagno is an academic researcher from University of Turin. The author has contributed to research in topics: Oxidative stress & Lipid peroxidation. The author has an hindex of 34, co-authored 68 publications receiving 8866 citations.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Oxidative stress increases expression and activity of BACE in NT2 neurons.

TL;DR: The results support the hypothesis that oxidative stress and A beta production are strictly interrelated events and suggest that inhibition of BACE may have a therapeutic effect synergic with antioxidant compounds.
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Beta-site APP cleaving enzyme up-regulation induced by 4-hydroxynonenal is mediated by stress-activated protein kinases pathways.

TL;DR: HNE, an oxidative stress mediator detected in vivo in the brains of Alzheimer's disease patients, may play a pathogenetic role in Alzheimer’s disease by selectively activating SAPK pathways and BACE‐1 that regulate the proteolytic processing of AβPP.
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Oxidative stress activates a positive feedback between the γ- and β-secretase cleavages of the β-amyloid precursor protein

TL;DR: It is shown that oxidative stress (OS) stimulates BACE1 expression by a mechanism requiring γ‐secretase activity involving the c‐jun N‐terminal kinase (JNK)/c‐jun pathway, thereby promoting production of pathological levels of amyloid β in AD.
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The up‐regulation of BACE1 mediated by hypoxia and ischemic injury: role of oxidative stress and HIF1α

TL;DR: This study significantly extends findings both in vitro, in differentiated SK‐N‐BE neuroblastoma cells, and in vivo, in rats subjected to cerebral ischemia, showing that hypoxia up‐regulates BACE1 expression through a biphasic mechanism, and strengthens the hypothesis that oxidative stress is a basic common mechanism of amyloid‐β accumulation.