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£126.42

Springer Polyglutamine Disorders: 1049 (Advances in Experimental Medicine and Biology, 1049)

Name: Polyglutamine Disorders: 1049 (Advances in Experimental Medicine and Biology, 1049)
Brand: Springer
Price: 126.42 GBP
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Neurology & Clinical Neurophysiology

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Description

This book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies’ development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression. Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington’s disease (HD); spinal–bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17). The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression. From the Back Cover This book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies’ development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression. Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington’s disease (HD); spinal–bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17). The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression. About the Author Clevio Nobrega Ph.D. and Luis Pereira de Almeida Ph.D. University of Coimbra, Center for Neurosciences and Cell Biology, FMUC, Coimbra, Portugal

Product Specifications

Brand: Springer
Format: hardcover
ASIN: 3319717782
Category: Books > Subjects > Health, Family & Lifestyle > Medical & Healthcare Practitioners > Internal Medicine > Neurology & Clinical Neurophysiology
Domain: Amazon UK
Release Date: 20 February 2018
Listed Since: 26 October 2017

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Springer Polyglutamine Disorders: 1049 (Advances in Experimental Medicine and Biology, 1049)

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