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Amyotrophic Lateral Sclerosis: A Focus on Disease Progression

Since amyotrophic lateral sclerosis (ALS) was discovered and described in 1869 as a neurodegenerative disease in which motor neuron death is induced, a wide range of biomarkers have been selected to identify therapeutic targets. ALS shares altered molecular pathways with other neurodegenerative dise...

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Detalles Bibliográficos
Autores principales: Calvo, Ana C., Manzano, Raquel, Mendonça, Deise M. F., Muñoz, María J., Zaragoza, Pilar, Osta, Rosario
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4137497/
https://www.ncbi.nlm.nih.gov/pubmed/25157374
http://dx.doi.org/10.1155/2014/925101
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author Calvo, Ana C.
Manzano, Raquel
Mendonça, Deise M. F.
Muñoz, María J.
Zaragoza, Pilar
Osta, Rosario
author_facet Calvo, Ana C.
Manzano, Raquel
Mendonça, Deise M. F.
Muñoz, María J.
Zaragoza, Pilar
Osta, Rosario
author_sort Calvo, Ana C.
collection PubMed
description Since amyotrophic lateral sclerosis (ALS) was discovered and described in 1869 as a neurodegenerative disease in which motor neuron death is induced, a wide range of biomarkers have been selected to identify therapeutic targets. ALS shares altered molecular pathways with other neurodegenerative diseases, such as Alzheimer's, Huntington's, and Parkinson's diseases. However, the molecular targets that directly influence its aggressive nature remain unknown. What is the first link in the neurodegenerative chain of ALS that makes this disease so peculiar? In this review, we will discuss the progression of the disease from the viewpoint of the potential biomarkers described to date in human and animal model samples. Finally, we will consider potential therapeutic strategies for ALS treatment and future, innovative perspectives.
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spelling pubmed-41374972014-08-25 Amyotrophic Lateral Sclerosis: A Focus on Disease Progression Calvo, Ana C. Manzano, Raquel Mendonça, Deise M. F. Muñoz, María J. Zaragoza, Pilar Osta, Rosario Biomed Res Int Review Article Since amyotrophic lateral sclerosis (ALS) was discovered and described in 1869 as a neurodegenerative disease in which motor neuron death is induced, a wide range of biomarkers have been selected to identify therapeutic targets. ALS shares altered molecular pathways with other neurodegenerative diseases, such as Alzheimer's, Huntington's, and Parkinson's diseases. However, the molecular targets that directly influence its aggressive nature remain unknown. What is the first link in the neurodegenerative chain of ALS that makes this disease so peculiar? In this review, we will discuss the progression of the disease from the viewpoint of the potential biomarkers described to date in human and animal model samples. Finally, we will consider potential therapeutic strategies for ALS treatment and future, innovative perspectives. Hindawi Publishing Corporation 2014 2014-08-03 /pmc/articles/PMC4137497/ /pubmed/25157374 http://dx.doi.org/10.1155/2014/925101 Text en Copyright © 2014 Ana C. Calvo et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Calvo, Ana C.
Manzano, Raquel
Mendonça, Deise M. F.
Muñoz, María J.
Zaragoza, Pilar
Osta, Rosario
Amyotrophic Lateral Sclerosis: A Focus on Disease Progression
title Amyotrophic Lateral Sclerosis: A Focus on Disease Progression
title_full Amyotrophic Lateral Sclerosis: A Focus on Disease Progression
title_fullStr Amyotrophic Lateral Sclerosis: A Focus on Disease Progression
title_full_unstemmed Amyotrophic Lateral Sclerosis: A Focus on Disease Progression
title_short Amyotrophic Lateral Sclerosis: A Focus on Disease Progression
title_sort amyotrophic lateral sclerosis: a focus on disease progression
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4137497/
https://www.ncbi.nlm.nih.gov/pubmed/25157374
http://dx.doi.org/10.1155/2014/925101
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