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Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target

Studies during the last two decades have provided new insights into the molecular mechanism of Alzheimer's disease (AD). One of the milestone findings in AD research was the demonstration that neurofibrillary degeneration characterized by tau pathology is central to the pathogenesis of AD and o...

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Detalles Bibliográficos
Autores principales: Gong, Cheng-Xin, Liu, Fei, Grundke-Iqbal, Inge, Iqbal, Khalid
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1559914/
https://www.ncbi.nlm.nih.gov/pubmed/17047304
http://dx.doi.org/10.1155/JBB/2006/31825
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author Gong, Cheng-Xin
Liu, Fei
Grundke-Iqbal, Inge
Iqbal, Khalid
author_facet Gong, Cheng-Xin
Liu, Fei
Grundke-Iqbal, Inge
Iqbal, Khalid
author_sort Gong, Cheng-Xin
collection PubMed
description Studies during the last two decades have provided new insights into the molecular mechanism of Alzheimer's disease (AD). One of the milestone findings in AD research was the demonstration that neurofibrillary degeneration characterized by tau pathology is central to the pathogenesis of AD and other tauopathies and that abnormal hyperphosphorylation of tau is pivotal to neurofibrillary degeneration. This article reviews the recent research advances in tau pathology and the underlying dysregulation of the protein phosphorylation/dephosphorylation system. An updated model of the mechanism of neurofibrillary degeneration is also presented, and a promising therapeutic target to treat AD by correcting dysregulation of protein phosphorylation/dephosphorylation is discussed.
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spelling pubmed-15599142006-10-10 Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target Gong, Cheng-Xin Liu, Fei Grundke-Iqbal, Inge Iqbal, Khalid J Biomed Biotechnol Review Article Studies during the last two decades have provided new insights into the molecular mechanism of Alzheimer's disease (AD). One of the milestone findings in AD research was the demonstration that neurofibrillary degeneration characterized by tau pathology is central to the pathogenesis of AD and other tauopathies and that abnormal hyperphosphorylation of tau is pivotal to neurofibrillary degeneration. This article reviews the recent research advances in tau pathology and the underlying dysregulation of the protein phosphorylation/dephosphorylation system. An updated model of the mechanism of neurofibrillary degeneration is also presented, and a promising therapeutic target to treat AD by correcting dysregulation of protein phosphorylation/dephosphorylation is discussed. Hindawi Publishing Corporation 2006 2006-03-21 /pmc/articles/PMC1559914/ /pubmed/17047304 http://dx.doi.org/10.1155/JBB/2006/31825 Text en Copyright © 2006 Cheng-Xin Gong et al. 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
Gong, Cheng-Xin
Liu, Fei
Grundke-Iqbal, Inge
Iqbal, Khalid
Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target
title Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target
title_full Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target
title_fullStr Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target
title_full_unstemmed Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target
title_short Dysregulation of Protein Phosphorylation/Dephosphorylation in Alzheimer's Disease: A Therapeutic Target
title_sort dysregulation of protein phosphorylation/dephosphorylation in alzheimer's disease: a therapeutic target
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1559914/
https://www.ncbi.nlm.nih.gov/pubmed/17047304
http://dx.doi.org/10.1155/JBB/2006/31825
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