La maladie de Parkinson en France (serveur d'exploration)

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Adaptive Preconditioning in Neurological Diseases - Therapeutic Insights from Proteostatic Perturbations

Identifieur interne : 000052 ( Hal/Corpus ); précédent : 000051; suivant : 000053

Adaptive Preconditioning in Neurological Diseases - Therapeutic Insights from Proteostatic Perturbations

Auteurs : B. Mollereau ; N. M. Rzechorzek ; B. D. Roussel ; M. Sedru ; D. Brink ; B. Bailly-Maitre ; F. Palladino ; D. B. Medinas ; P. M. Domingos ; S. Hunot ; S. Chandran ; S. Birman ; T. Baron ; D. Vivien ; C. B. Duarte ; H. D. Ryoo ; H. Steller ; F. Urano ; E. Chevet ; G. Kroemer ; A. Ciechanover ; E. J. Calabrese ; R. J. Kaufman ; C. Hetz

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RBID : Hal:hal-01282346

English descriptors

Abstract

In neurological disorders, both acute and chronic neural stress can disrupt cellular proteostasis, resulting in the generation of pathological protein. However in most cases, neurons adapt to these proteostatic perturbations by activating a range of cellular protective and repair responses, thus maintaining cell function. These interconnected adaptive mechanisms comprise a 'proteostasis network' and include the unfolded protein response, the ubiquitin proteasome system and autophagy. Interestingly, several recent studies have shown that these adaptive responses can be stimulated by preconditioning treatments, which confer resistance to a subsequent toxic challenge - the phenomenon known as hormesis. In this review we discuss the impact of adaptive stress responses stimulated in diverse human neuropathologies including Parkinson´s disease, Wolfram syndrome, brain ischemia, and brain cancer. Further, we examine how these responses - and the molecular pathways they recruit - might be exploited for therapeutic gain

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DOI: 10.1016/j.brainres.2016.02.033

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Hal:hal-01282346

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<idno type="DOI">10.1016/j.brainres.2016.02.033</idno>
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<title level="j">Brain Research</title>
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<term> ER stress</term>
<term> Hormesis</term>
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<term> Parkinson</term>
<term> Proteasome</term>
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<div type="abstract" xml:lang="en">In neurological disorders, both acute and chronic neural stress can disrupt cellular proteostasis, resulting in the generation of pathological protein. However in most cases, neurons adapt to these proteostatic perturbations by activating a range of cellular protective and repair responses, thus maintaining cell function. These interconnected adaptive mechanisms comprise a 'proteostasis network' and include the unfolded protein response, the ubiquitin proteasome system and autophagy. Interestingly, several recent studies have shown that these adaptive responses can be stimulated by preconditioning treatments, which confer resistance to a subsequent toxic challenge - the phenomenon known as hormesis. In this review we discuss the impact of adaptive stress responses stimulated in diverse human neuropathologies including Parkinson´s disease, Wolfram syndrome, brain ischemia, and brain cancer. Further, we examine how these responses - and the molecular pathways they recruit - might be exploited for therapeutic gain</div>
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<forename type="first">E. J.</forename>
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<forename type="first">R. J.</forename>
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<biblScope unit="issue">B</biblScope>
<biblScope unit="pp">603–616</biblScope>
<date type="datePub">2016-02</date>
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<idno type="doi">10.1016/j.brainres.2016.02.033</idno>
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<langUsage>
<language ident="en">English</language>
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<keywords scheme="author">
<term xml:lang="en"> Parkinson</term>
<term xml:lang="en"> Hormesis</term>
<term xml:lang="en"> Ischemia</term>
<term xml:lang="en">Autophagy</term>
<term xml:lang="en"> ER stress</term>
<term xml:lang="en"> Proteasome</term>
</keywords>
<classCode scheme="halDomain" n="sdv">Life Sciences [q-bio]</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en">In neurological disorders, both acute and chronic neural stress can disrupt cellular proteostasis, resulting in the generation of pathological protein. However in most cases, neurons adapt to these proteostatic perturbations by activating a range of cellular protective and repair responses, thus maintaining cell function. These interconnected adaptive mechanisms comprise a 'proteostasis network' and include the unfolded protein response, the ubiquitin proteasome system and autophagy. Interestingly, several recent studies have shown that these adaptive responses can be stimulated by preconditioning treatments, which confer resistance to a subsequent toxic challenge - the phenomenon known as hormesis. In this review we discuss the impact of adaptive stress responses stimulated in diverse human neuropathologies including Parkinson´s disease, Wolfram syndrome, brain ischemia, and brain cancer. Further, we examine how these responses - and the molecular pathways they recruit - might be exploited for therapeutic gain</abstract>
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