Insights into synaptic function from mouse models of human cognitive disorders
Identifieur interne : 003529 ( Pmc/Corpus ); précédent : 003528; suivant : 003530Insights into synaptic function from mouse models of human cognitive disorders
Auteurs : Jessica L. Banko ; Justin Trotter ; Edwin J. WeeberSource :
- Future neurology [ 1479-6708 ] ; 2011.
Abstract
Modern approaches to the investigation of the molecular mechanisms underlying human cognitive disease often include multidisciplinary examination of animal models engineered with specific mutations that spatially and temporally restrict expression of a gene of interest. This approach not only makes possible the development of animal models that demonstrate phenotypic similarities to their respective human disorders, but has also allowed for significant progress towards understanding the processes that mediate synaptic function and memory formation in the nondiseased state. Examples of successful mouse models where genetic manipulation of the mouse resulted in recapitulation of the symptomatology of the human disorder and was used to significantly expand our understanding of the molecular mechanisms underlying normal synaptic plasticity and memory formation are discussed in this article. These studies have broadened our knowledge of several signal transduction cascades that function throughout life to mediate synaptic physiology. Defining these events is key for developing therapies to address disorders of cognitive ability.
Url:
DOI: 10.2217/fnl.10.80
PubMed: 25083141
PubMed Central: 4114080
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PMC:4114080Le document en format XML
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<author><name sortKey="Banko, Jessica L" sort="Banko, Jessica L" uniqKey="Banko J" first="Jessica L" last="Banko">Jessica L. Banko</name>
<affiliation><nlm:aff id="A1">Department of Molecular Medicine, USF Health Byrd Alzheimer’s Research Institute, University of South Florida, Tampa, FL, USA</nlm:aff>
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<front><div type="abstract" xml:lang="en"><p id="P1">Modern approaches to the investigation of the molecular mechanisms underlying human cognitive disease often include multidisciplinary examination of animal models engineered with specific mutations that spatially and temporally restrict expression of a gene of interest. This approach not only makes possible the development of animal models that demonstrate phenotypic similarities to their respective human disorders, but has also allowed for significant progress towards understanding the processes that mediate synaptic function and memory formation in the nondiseased state. Examples of successful mouse models where genetic manipulation of the mouse resulted in recapitulation of the symptomatology of the human disorder and was used to significantly expand our understanding of the molecular mechanisms underlying normal synaptic plasticity and memory formation are discussed in this article. These studies have broadened our knowledge of several signal transduction cascades that function throughout life to mediate synaptic physiology. Defining these events is key for developing therapies to address disorders of cognitive ability.</p>
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<journal-id journal-id-type="nlm-ta">Future Neurol</journal-id>
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<contrib-group><contrib contrib-type="author"><name><surname>Banko</surname>
<given-names>Jessica L</given-names>
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<contrib contrib-type="author"><name><surname>Weeber</surname>
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<aff id="A1"><label>1</label>
Department of Molecular Medicine, USF Health Byrd Alzheimer’s Research Institute, University of South Florida, Tampa, FL, USA</aff>
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Department of Molecular Pharmacology & Physiology, USF Health Byrd Alzheimer’s Research Institute, University of South Florida, 4001 East Fletcher Ave, Tampa, FL 33612, USA</aff>
<author-notes><corresp id="cor1"><label>†</label>
Author for correspondence: Tel.: +1 813 396 9995, Fax:+1 813 971 0373, <email>eweeber@health.usf.edu</email>
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<pub-date pub-type="nihms-submitted"><day>12</day>
<month>9</month>
<year>2013</year>
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<year>2011</year>
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<pub-date pub-type="pmc-release"><day>29</day>
<month>7</month>
<year>2014</year>
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<volume>6</volume>
<issue>1</issue>
<fpage>113</fpage>
<lpage>125</lpage>
<pmc-comment>elocation-id from pubmed: 10.2217/fnl.10.80</pmc-comment>
<permissions><copyright-statement>© 2011 Future Medicine Ltd</copyright-statement>
<copyright-year>2011</copyright-year>
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<abstract><p id="P1">Modern approaches to the investigation of the molecular mechanisms underlying human cognitive disease often include multidisciplinary examination of animal models engineered with specific mutations that spatially and temporally restrict expression of a gene of interest. This approach not only makes possible the development of animal models that demonstrate phenotypic similarities to their respective human disorders, but has also allowed for significant progress towards understanding the processes that mediate synaptic function and memory formation in the nondiseased state. Examples of successful mouse models where genetic manipulation of the mouse resulted in recapitulation of the symptomatology of the human disorder and was used to significantly expand our understanding of the molecular mechanisms underlying normal synaptic plasticity and memory formation are discussed in this article. These studies have broadened our knowledge of several signal transduction cascades that function throughout life to mediate synaptic physiology. Defining these events is key for developing therapies to address disorders of cognitive ability.</p>
</abstract>
<kwd-group><kwd>Alzheimer’s disease</kwd>
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<kwd>hippocampus</kwd>
<kwd>knockout mouse</kwd>
<kwd>neurofibromatosis type 1</kwd>
<kwd>Reelin</kwd>
<kwd>Rubinstein-Taybi syndrome</kwd>
<kwd>secretin</kwd>
<kwd>synaptic plasticity</kwd>
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