Review: Cell cycle aberrations and neurodegeneration
Identifieur interne : 002862 ( Main/Corpus ); précédent : 002861; suivant : 002863Review: Cell cycle aberrations and neurodegeneration
Auteurs : D. J. Bonda ; V. P. Baji ; B. Spremo-Potparevic ; G. Casadesus ; X. Zhu ; M. A. Smith ; H. LeeSource :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 2010-04.
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Abstract
D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.
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DOI: 10.1111/j.1365-2990.2010.01064.x
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<front><div type="abstract" xml:lang="en">D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</div>
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Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</abstract>
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<abstractGroup><abstract type="main" xml:lang="en"><p>D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) <i>Neuropathology and Applied Neurobiology</i>
<b>36,</b>
157–163
<b>Cell cycle aberrations and neurodegeneration</b>
</p>
<p>The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</p>
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<name type="personal"><namePart type="given">D. J.</namePart>
<namePart type="family">Bonda</namePart>
<affiliation>Departments of Pathology and</affiliation>
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<name type="personal"><namePart type="given">V. P.</namePart>
<namePart type="family">Bajić</namePart>
<affiliation>Institute of Biomedical Research, Galenika a.d., and</affiliation>
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<affiliation>Department of Physiology, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia</affiliation>
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<name type="personal"><namePart type="given">G.</namePart>
<namePart type="family">Casadesus</namePart>
<affiliation>Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA;</affiliation>
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<affiliation>Departments of Pathology and</affiliation>
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<name type="personal"><namePart type="given">M. A.</namePart>
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<affiliation>Departments of Pathology and</affiliation>
<description>Correspondence: Mark A. Smith, Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA. Tel: +1 216 368 3670; Fax: +1 216 368 8964; E‐mail: </description>
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<dateIssued encoding="w3cdtf">2010-04</dateIssued>
<edition>Received 30 September 2009Accepted after revision 22 December 2009Published online Article Accepted on 6 January 2010</edition>
<copyrightDate encoding="w3cdtf">2010</copyrightDate>
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<abstract lang="en">D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</abstract>
<subject lang="en"><genre>Keywords</genre>
<topic>Alzheimer disease</topic>
<topic>cell cycle re‐entry</topic>
<topic>mitotic insult</topic>
<topic>mitotic steady state</topic>
<topic>oxidative stress</topic>
</subject>
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<identifier type="ISSN">0305-1846</identifier>
<identifier type="eISSN">1365-2990</identifier>
<identifier type="DOI">10.1111/(ISSN)1365-2990</identifier>
<identifier type="PublisherID">NAN</identifier>
<part><date>2010</date>
<detail type="volume"><caption>vol.</caption>
<number>36</number>
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<detail type="issue"><caption>no.</caption>
<number>2</number>
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<extent unit="pages"><start>157</start>
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