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 inExperimental neurobiology Vol. 22; no. 4; pp. 244 - 248
Main Authors Park, Joongkyu, Chung, Kwang Chul
Format Journal Article
LanguageEnglish
Published Korea (South) The Korean Society for Brain and Neural Science 01.12.2013
한국뇌신경과학회
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ISSN1226-2560
2093-8144
DOI10.5607/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.
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
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Issue 4
Keywords down syndrome
neuritogenesis
cytoskeletal proteins
synaptogenesis
Dyrk1A
Language English
License This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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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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