Intracellular Traffic and Neurodegenerative Disorders - Couverture rigide

 
9783540879404: Intracellular Traffic and Neurodegenerative Disorders

Synopsis

Neurodegenerative disorders are common and devastating. Rationally, the most effective treatments will target pathogenetic mechanisms. While alternative - proaches, based on alleviating the symptoms of patients with Alzheimer disease, Parkinson disease, Huntington disease, prion disorders or amyotrophic lateral sc- rosis, can be expected to reduce suffering, studies of pathogenesis of these a- related disorders will be most important for enabling early diagnosis and the creation of preventative and curative treatments. It is in this context that a recent IPSEN rd meeting (The 23 Colloque Medecine ´ et Recherche, April 28, 2008) focused on a role for disruption of intracellular traf?cking in neurodegenerative disorders. The meeting captured emerging insights into pathogenesis from disrupted traf?cking and processing of proteins implicated in age-related degeneration. Protein folding, traf?cking and signaling were the principal topics covered at the meeting. Importantly, the presenters pointed to the importantly intersection of these themes. While the proteolytic processing of APP into its toxic product, the A? peptide, is an intensive focus of work in many laboratories, it is only relatively recently that investigators have begun to examine in depth the cellular compartments and traf?cking events that mediate APP processing and how derangement of tr- ?cking pathways could impact them.

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Présentation de l'éditeur

Many adult onset neurodegenerative diseases arise from the accumulation of misfolded peptides. This book examines the role sub-cellular trafficking pathways play in the pathological accumulation of these misfolded proteins and in attempts to clear them.

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Autres éditions populaires du même titre

9783642099724: Intracellular Traffic and Neurodegenerative Disorders

Edition présentée

ISBN 10 :  3642099726 ISBN 13 :  9783642099724
Editeur : Springer, 2010
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