New Perspectives of Dyrk1A Role in Neurogenesis and Neuropathologic Features of Down Syndrome
Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration in neurogenesis and synaptogenesis and early onset of A...
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Published in | Experimental neurobiology Vol. 22; no. 4; pp. 244 - 248 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
The Korean Society for Brain and Neural Science
01.12.2013
한국뇌신경과학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1226-2560 2093-8144 |
DOI | 10.5607/en.2013.22.4.244 |
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Abstract | Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration in neurogenesis and synaptogenesis and early onset of Alzheimer's disease (AD)-like symptoms. Triplication of all or a part of human chromosome 21, especially the 21q22.1~21q22.3 region called 'Down syndrome critical region (DSCR)', has been considered as the main cause of DS. One gene product of DSCR, dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A), has been highlighted as a key contributor to the neural consequences of DS. This minireview summarizes accumulating recent reports about Dyrk1A involvement in the neuritogenesis, synaptogenesis, and AD-like neurofibrillary tangle formation, which is mainly focusing on Dyrk1A-mediated regulation of cytoskeletal proteins, such as tubulin, actin, and microtubule-associated protein tau. Understanding the molecular mechanisms of these phenomena may provide us a rational for new preventive and therapeutic treatment of DS. |
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AbstractList | Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment,and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration inneurogenesis and synaptogenesis and early onset of Alzheimer’s disease (AD)-like symptoms. Triplication of all or a part of humanchromosome 21, especially the 21q22.1~21q22.3 region called ‘Down syndrome critical region (DSCR)’, has been considered asthe main cause of DS. One gene product of DSCR, dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A), hasbeen highlighted as a key contributor to the neural consequences of DS. This minireview summarizes accumulating recent reportsabout Dyrk1A involvement in the neuritogenesis, synaptogenesis, and AD-like neurofibrillary tangle formation, which is mainlyfocusing on Dyrk1A-mediated regulation of cytoskeletal proteins, such as tubulin, actin, and microtubule-associated protein tau.
Understanding the molecular mechanisms of these phenomena may provide us a rational for new preventive and therapeutictreatment of DS. KCI Citation Count: 0 Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration in neurogenesis and synaptogenesis and early onset of Alzheimer's disease (AD)-like symptoms. Triplication of all or a part of human chromosome 21, especially the 21q22.1~21q22.3 region called 'Down syndrome critical region (DSCR)', has been considered as the main cause of DS. One gene product of DSCR, dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A), has been highlighted as a key contributor to the neural consequences of DS. This minireview summarizes accumulating recent reports about Dyrk1A involvement in the neuritogenesis, synaptogenesis, and AD-like neurofibrillary tangle formation, which is mainly focusing on Dyrk1A-mediated regulation of cytoskeletal proteins, such as tubulin, actin, and microtubule-associated protein tau. Understanding the molecular mechanisms of these phenomena may provide us a rational for new preventive and therapeutic treatment of DS.Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration in neurogenesis and synaptogenesis and early onset of Alzheimer's disease (AD)-like symptoms. Triplication of all or a part of human chromosome 21, especially the 21q22.1~21q22.3 region called 'Down syndrome critical region (DSCR)', has been considered as the main cause of DS. One gene product of DSCR, dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A), has been highlighted as a key contributor to the neural consequences of DS. This minireview summarizes accumulating recent reports about Dyrk1A involvement in the neuritogenesis, synaptogenesis, and AD-like neurofibrillary tangle formation, which is mainly focusing on Dyrk1A-mediated regulation of cytoskeletal proteins, such as tubulin, actin, and microtubule-associated protein tau. Understanding the molecular mechanisms of these phenomena may provide us a rational for new preventive and therapeutic treatment of DS. Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory. The brains with DS also display many neuropathological features including alteration in neurogenesis and synaptogenesis and early onset of Alzheimer's disease (AD)-like symptoms. Triplication of all or a part of human chromosome 21, especially the 21q22.1~21q22.3 region called 'Down syndrome critical region (DSCR)', has been considered as the main cause of DS. One gene product of DSCR, dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A), has been highlighted as a key contributor to the neural consequences of DS. This minireview summarizes accumulating recent reports about Dyrk1A involvement in the neuritogenesis, synaptogenesis, and AD-like neurofibrillary tangle formation, which is mainly focusing on Dyrk1A-mediated regulation of cytoskeletal proteins, such as tubulin, actin, and microtubule-associated protein tau. Understanding the molecular mechanisms of these phenomena may provide us a rational for new preventive and therapeutic treatment of DS. |
Author | Chung, Kwang Chul Park, Joongkyu |
AuthorAffiliation | 1 Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Korea 2 Program in Cellular Neuroscience, Neurodegeneration and Repair (CNNR), Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA |
AuthorAffiliation_xml | – name: 1 Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Korea – name: 2 Program in Cellular Neuroscience, Neurodegeneration and Repair (CNNR), Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA |
Author_xml | – sequence: 1 givenname: Joongkyu surname: Park fullname: Park, Joongkyu organization: Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Korea, Program in Cellular Neuroscience, Neurodegeneration and Repair (CNNR), Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA – sequence: 2 givenname: Kwang Chul surname: Chung fullname: Chung, Kwang Chul organization: Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Korea |
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Snippet | Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment, and deficits in learning and memory.... Down syndrome (DS) is one of the most common genetic disorders accompanying with mental retardation, cognitive impairment,and deficits in learning and memory.... |
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Title | New Perspectives of Dyrk1A Role in Neurogenesis and Neuropathologic Features of Down Syndrome |
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