Experimental therapeutics in transgenic mouse models of Huntington's disease
Identifieur interne : 001B19 ( Main/Corpus ); précédent : 001B18; suivant : 001B20Experimental therapeutics in transgenic mouse models of Huntington's disease
Auteurs : M. Flint Beal ; Robert J. FerranteSource :
- Nature Reviews Neuroscience [ 1471-003X ] ; 2004-05.
Abstract
Despite important advances in understanding and elucidating the molecular and mechanistic pathways that mediate progression in Huntington's disease (HD), effective pharmacotherapy remains elusive. Insights into disease pathogenesis have come from studies using tissue culture, yeast, Caenorhabditis elegans, Drosophila melanogaster and transgenic mouse models. Here, we present a brief overview of HD pathogenesis and discuss the efficacy of therapeutic agents in transgenic mouse models of HD. We conclude by considering issues that affect the translation of findings in transgenic mouse models of HD to human clinical trials.
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DOI: 10.1038/nrn1386
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Flint</forename><surname>Beal</surname></persName><email>fbeal@med.cornell.edu</email><note type="biography">M. Flint Beal is the Anne Parrish Titzell Professor and Chairman of the Department of Neurology and Neuroscience at the Weill Medical College of Cornell University, and Director of the Neurology Service at the New York Presbyterian Cornell Campus. Beal received his medical degree from the University of Virginia in 1976. He did his internship and first year residency in medicine at Cornell, New York, before completing his residency in neurology at the Massachusetts General Hospital. He joined the neurology faculty at Harvard in 1983, and was Professor of Neurology at Harvard Medical School and Chief of the Neurochemistry Laboratory at Massachusetts General Hospital before moving to Cornell. Beal's research has focused on the mechanism of neuronal degeneration in Alzheimer's, Huntington's and Parkinson's diseases and amyotrophic lateral sclerosis.</note><affiliation>M. Flint Beal is the Anne Parrish Titzell Professor and Chairman of the Department of Neurology and Neuroscience at the Weill Medical College of Cornell University, and Director of the Neurology Service at the New York Presbyterian Cornell Campus. Beal received his medical degree from the University of Virginia in 1976. He did his internship and first year residency in medicine at Cornell, New York, before completing his residency in neurology at the Massachusetts General Hospital. He joined the neurology faculty at Harvard in 1983, and was Professor of Neurology at Harvard Medical School and Chief of the Neurochemistry Laboratory at Massachusetts General Hospital before moving to Cornell. Beal's research has focused on the mechanism of neuronal degeneration in Alzheimer's, Huntington's and Parkinson's diseases and amyotrophic lateral sclerosis.</affiliation><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F610, 525 East 68th Street, New York, NY 10021 USA.</affiliation></author><author><persName><forename type="first">Robert J.</forename><surname>Ferrante</surname></persName><note type="biography">Robert J. Ferrante is the Director of the Experimental Neuropathology Laboratory in the Geriatrics Research Education and Clinical Center at the Edith Nourse VA Medical Center. He is an associate professor of the neurology, pathology and psychiatry departments at Boston University School of Medicine. He obtained his Ph.D. from Boston University Medical School. His interests are neuropathology and the mechanisms of neurodegeneration as related to clinical and experimental neurology. His laboratory presently focuses on preclinical translational drug trials in animal models of neurological disorders, particularly Huntington's disease and amyotrophic lateral sclerosis.</note><affiliation>Robert J. Ferrante is the Director of the Experimental Neuropathology Laboratory in the Geriatrics Research Education and Clinical Center at the Edith Nourse VA Medical Center. He is an associate professor of the neurology, pathology and psychiatry departments at Boston University School of Medicine. He obtained his Ph.D. from Boston University Medical School. His interests are neuropathology and the mechanisms of neurodegeneration as related to clinical and experimental neurology. His laboratory presently focuses on preclinical translational drug trials in animal models of neurological disorders, particularly Huntington's disease and amyotrophic lateral sclerosis.</affiliation><affiliation>Geriatric Research Education and Clinical Center, Bedford VA Medical Center, Bedford, Massachusetts and the Departments of Neurology, Pathology and Psychiatry, Boston University School of Medicine, Boston, Massachusetts 02118, USA.</affiliation></author></analytic><monogr><title level="j">Nature Reviews Neuroscience</title><idno type="pISSN">1471-003X</idno><idno type="eISSN">1471-0048</idno><imprint><publisher>Nature Publishing Group</publisher><date type="published" when="2004-05"></date><biblScope unit="volume">5</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="373">373</biblScope><biblScope unit="page" to="384">384</biblScope></imprint></monogr><idno type="istex">ADD21E9CF568E6B1C32613EC8395BE7F7A304735</idno><idno type="DOI">10.1038/nrn1386</idno><idno type="ArticleID">nrn1386</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Despite important advances in understanding and elucidating the molecular and mechanistic pathways that mediate progression in Huntington's disease (HD), effective pharmacotherapy remains elusive. 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Flint</fnm><snm>Beal</snm><inits>M F</inits><orf rid="a1"></orf><corf rid="c1"></corf><bio><p>M. Flint Beal is the Anne Parrish Titzell Professor and Chairman of the Department of Neurology and Neuroscience at the Weill Medical College of Cornell University, and Director of the Neurology Service at the New York Presbyterian Cornell Campus. Beal received his medical degree from the University of Virginia in 1976. He did his internship and first year residency in medicine at Cornell, New York, before completing his residency in neurology at the Massachusetts General Hospital. He joined the neurology faculty at Harvard in 1983, and was Professor of Neurology at Harvard Medical School and Chief of the Neurochemistry Laboratory at Massachusetts General Hospital before moving to Cornell. Beal's research has focused on the mechanism of neuronal degeneration in Alzheimer's, Huntington's and Parkinson's diseases and amyotrophic lateral sclerosis.</p></bio></cau><au><fnm>Robert J.</fnm><snm>Ferrante</snm><inits>R J</inits><orf rid="a2"></orf><bio><p>Robert J. Ferrante is the Director of the Experimental Neuropathology Laboratory in the Geriatrics Research Education and Clinical Center at the Edith Nourse VA Medical Center. He is an associate professor of the neurology, pathology and psychiatry departments at Boston University School of Medicine. He obtained his Ph.D. from Boston University Medical School. His interests are neuropathology and the mechanisms of neurodegeneration as related to clinical and experimental neurology. His laboratory presently focuses on preclinical translational drug trials in animal models of neurological disorders, particularly Huntington's disease and amyotrophic lateral sclerosis.</p></bio></au><aff><oid id="a1"></oid><org>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F610</org>, <street>525 East 68th Street</street>, <cty>New York</cty>, <st>NY</st> <zip>10021</zip> <cny>USA</cny>.</aff><aff><oid id="a2"></oid><org>Geriatric Research Education and Clinical Center, Bedford VA Medical Center, Bedford, Massachusetts and the Departments of Neurology, Pathology and Psychiatry, Boston University School of Medicine</org>, <cty>Boston</cty>, <st>Massachusetts</st> <zip>02118</zip>, <cny>USA</cny>.</aff><caff><coid id="c1"></coid><email>fbeal@med.cornell.edu</email></caff></aug><execsumm><p><list id="l1" type="bullet"><li>Huntingtin is a predominantly cytoplasmic protein that is found in neurons throughout the brain. The precise mechanism by which mutant huntingtin causes Huntington's disease (HD) is unknown but seems to be gain-of-function. The gene that encodes this protein can be mutated by expansion of a trinucleotide CAG repeat that encodes glutamine.</li><li>N-terminal fragments of mutant huntingtin form toxic protein aggregates in neurons. Mutant huntingtin causes progressive neuronal dysfunction and death — HD is ultimately lethal.</li><li>There are several different transgenic mouse models of HD that have enhanced the study of this disorder and the capacity to test promising therapeutics. Mouse models fall into three categories: (1) those that express full-length mutant human huntingtin; (2) those that express fragments of the mutant human <i>huntingtin</i> gene; and (3) those with CAG repeats inserted into the murine <i>huntingtin</i> gene.</li><li>These mouse models have been used to investigate the role in HD of several processes that might be targeted therapeutically. These processes include: proteolysis of huntingtin; aggregation of huntingtin; apoptosis; transcriptional dysregulation; mitochondrial dysfunction; excitotoxicity; inflammation and oxidative damage; and transglutaminase activity.</li><li>Vaccination against toxic proteins and transplantation of healthy brain tissue are two approaches to treatment that are under investigation.</li><li>There is no consensus as to which type of mouse model is the best model of human HD. There have been few clinical trials of treatments in humans on which to base a comparative conclusion.</li></list></p></execsumm><abs><p>Despite important advances in understanding and elucidating the molecular and mechanistic pathways that mediate progression in Huntington's disease (HD), effective pharmacotherapy remains elusive. Insights into disease pathogenesis have come from studies using tissue culture, yeast, <i>Caenorhabditis elegans</i>, <i>Drosophila melanogaster</i> and transgenic mouse models. Here, we present a brief overview of HD pathogenesis and discuss the efficacy of therapeutic agents in transgenic mouse models of HD. We conclude by considering issues that affect the translation of findings in transgenic mouse models of HD to human clinical trials.</p></abs></fm></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="eng"><title>Experimental therapeutics in transgenic mouse models of Huntington's disease</title></titleInfo><titleInfo type="alternative" lang="eng" contentType="CDATA"><title>Experimental therapeutics in transgenic mouse models of Huntington's disease</title></titleInfo><name type="personal"><namePart type="given">M. Flint</namePart><namePart type="family">Beal</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F610, 525 East 68th Street, New York, NY 10021 USA.</affiliation><affiliation>E-mail: fbeal@med.cornell.edu</affiliation><role><roleTerm type="text">author</roleTerm></role><description>M. Flint Beal is the Anne Parrish Titzell Professor and Chairman of the Department of Neurology and Neuroscience at the Weill Medical College of Cornell University, and Director of the Neurology Service at the New York Presbyterian Cornell Campus. Beal received his medical degree from the University of Virginia in 1976. He did his internship and first year residency in medicine at Cornell, New York, before completing his residency in neurology at the Massachusetts General Hospital. 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He is an associate professor of the neurology, pathology and psychiatry departments at Boston University School of Medicine. He obtained his Ph.D. from Boston University Medical School. His interests are neuropathology and the mechanisms of neurodegeneration as related to clinical and experimental neurology. 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