Progressive sensorimotor impairment is not associated with reduced dopamine and high energy phosphate donors in a model of ataxia-telangiectasia
Identifieur interne : 000994 ( PascalFrancis/Corpus ); précédent : 000993; suivant : 000995Progressive sensorimotor impairment is not associated with reduced dopamine and high energy phosphate donors in a model of ataxia-telangiectasia
Auteurs : Howard T. J. Mount ; Jean-Claude Martel ; Paul Fluit ; YINGJI WU ; Eleanor Gallo-Hendrikx ; Cristina Cosi ; Marc R. MarienSource :
- Journal of neurochemistry [ 0022-3042 ] ; 2004.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Ataxia-telangiectasia (A-T) is a genetic disease, associated with progressive motor impairment and a lack of functional ATM protein. It has been reported that immunoreactive tyrosine hydroxylase and dopamine transporter are reduced in an Atm-/- mouse model of A-T. These observations led to a hypothesis that A-T is associated with loss of nigrostriatal dopamine and prompted the launch of clinical trials to evaluate a therapeutic utility of the anti-parkinsonian drug, L-DOPA. To test for dopamine depletion more directly, we measured regional levels of monoamines and their metabolites in the Atm-/-mouse brain. We also measured levels of NAD+, a cofactor for dopamine biosynthesis and substrate of the DNA damage surveillance enzyme, poly(ADP-ribose) polymerase (PARP). Constitutive activation of PARP has been posited to cause NAD+ depletion. We observed no reduction in monoamine transmitters and no depletion of NAD+, or other high energy phosphate donors in the adult Atm-/- cerebellum, striatum, or ventral mesencephalon. However, our studies did reveal a progressive sensorimotor impairment in Atm-/-mice that may serve as a relevant proxy for progressive neurological impairment in the human disease. Our results call into question the involvement of dopamine in A-T and the therapeutic strategy of enhancing dopaminergic function with L-DOPA.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
| NO : | PASCAL 04-0345628 INIST |
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| ET : | Progressive sensorimotor impairment is not associated with reduced dopamine and high energy phosphate donors in a model of ataxia-telangiectasia |
| AU : | MOUNT (Howard T. J.); MARTEL (Jean-Claude); FLUIT (Paul); YINGJI WU; GALLO-HENDRIKX (Eleanor); COSI (Cristina); MARIEN (Marc R.) |
| AF : | Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto/Toronto, Ontario/Canada (1 aut., 3 aut., 4 aut., 5 aut.); Division of Neurology, Department of Medicine, University of Toronto/Toronto, Ontario/Canada (1 aut.); Institut de Reclterche Pierre Fabre/Castres/France (2 aut., 6 aut., 7 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2004; Vol. 88; No. 6; Pp. 1449-1454; Bibl. 32 ref. |
| LA : | Anglais |
| EA : | Ataxia-telangiectasia (A-T) is a genetic disease, associated with progressive motor impairment and a lack of functional ATM protein. It has been reported that immunoreactive tyrosine hydroxylase and dopamine transporter are reduced in an Atm-/- mouse model of A-T. These observations led to a hypothesis that A-T is associated with loss of nigrostriatal dopamine and prompted the launch of clinical trials to evaluate a therapeutic utility of the anti-parkinsonian drug, L-DOPA. To test for dopamine depletion more directly, we measured regional levels of monoamines and their metabolites in the Atm-/-mouse brain. We also measured levels of NAD+, a cofactor for dopamine biosynthesis and substrate of the DNA damage surveillance enzyme, poly(ADP-ribose) polymerase (PARP). Constitutive activation of PARP has been posited to cause NAD+ depletion. We observed no reduction in monoamine transmitters and no depletion of NAD+, or other high energy phosphate donors in the adult Atm-/- cerebellum, striatum, or ventral mesencephalon. However, our studies did reveal a progressive sensorimotor impairment in Atm-/-mice that may serve as a relevant proxy for progressive neurological impairment in the human disease. Our results call into question the involvement of dopamine in A-T and the therapeutic strategy of enhancing dopaminergic function with L-DOPA. |
| CC : | 002B17G; 002B17A01 |
| FD : | Dopamine; Déplétion; Biosynthèse; Voie nigrostriatale; NAD+ ADP-ribosyltransferase; Tyrosine 3-monooxygenase; Coordination sensorimotrice; Ataxie télangiectasie; Posture; Cervelet; Parkinson maladie; Souris; Animal; NAD+ |
| FG : | Pentosyltransferases; Glycosyltransferases; Transferases; Enzyme; Oxidoreductases; Neurotransmetteur; Catécholamine; Système nerveux pathologie; Appareil circulatoire pathologie; Vaisseau sanguin pathologie; Oeil pathologie; Peau pathologie; Immunopathologie; Maladie héréditaire; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata |
| ED : | Dopamine; Depletion; Biosynthesis; Nigrostriatal pathway; NAD+ ADP-ribosyltransferase; Tyrosine 3-monooxygenase; Sensorimotor coordination; Ataxia telangiectasia; Posture; Cerebellum; Parkinson disease; Mouse; Animal; NAD+ |
| EG : | Pentosyltransferases; Glycosyltransferases; Transferases; Enzyme; Oxidoreductases; Neurotransmitter; Catecholamine; Nervous system diseases; Cardiovascular disease; Vascular disease; Eye disease; Skin disease; Immunopathology; Genetic disease; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata |
| SD : | Dopamina; Depleción; Biosíntesis; Vía nigroestriatal; NAD+ ADP-ribosyltransferase; Tyrosine 3-monooxygenase; Coordinación sensoriomotora; Ataxia telangiectasia; Postura; Cerebelo; Parkinson enfermedad; Ratón; Animal |
| LO : | INIST-4037.354000111456470160 |
| ID : | 04-0345628 |
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Mount</name><affiliation><inist:fA14 i1="01"><s1>Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Division of Neurology, Department of Medicine, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Martel, Jean Claude" sort="Martel, Jean Claude" uniqKey="Martel J" first="Jean-Claude" last="Martel">Jean-Claude Martel</name><affiliation><inist:fA14 i1="03"><s1>Institut de Reclterche Pierre Fabre</s1><s2>Castres</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Fluit, Paul" sort="Fluit, Paul" uniqKey="Fluit P" first="Paul" last="Fluit">Paul Fluit</name><affiliation><inist:fA14 i1="01"><s1>Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Yingji Wu" sort="Yingji Wu" uniqKey="Yingji Wu" last="Yingji Wu">YINGJI WU</name><affiliation><inist:fA14 i1="01"><s1>Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Gallo Hendrikx, Eleanor" sort="Gallo Hendrikx, Eleanor" uniqKey="Gallo Hendrikx E" first="Eleanor" last="Gallo-Hendrikx">Eleanor Gallo-Hendrikx</name><affiliation><inist:fA14 i1="01"><s1>Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Cosi, Cristina" sort="Cosi, Cristina" uniqKey="Cosi C" first="Cristina" last="Cosi">Cristina Cosi</name><affiliation><inist:fA14 i1="03"><s1>Institut de Reclterche Pierre Fabre</s1><s2>Castres</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Marien, Marc R" sort="Marien, Marc R" uniqKey="Marien M" first="Marc R." last="Marien">Marc R. Marien</name><affiliation><inist:fA14 i1="03"><s1>Institut de Reclterche Pierre Fabre</s1><s2>Castres</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2004">2004</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Ataxia telangiectasia</term><term>Biosynthesis</term><term>Cerebellum</term><term>Depletion</term><term>Dopamine</term><term>Mouse</term><term>Nigrostriatal pathway</term><term>Parkinson disease</term><term>Posture</term><term>Sensorimotor coordination</term><term>Tyrosine 3-monooxygenase</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dopamine</term><term>Déplétion</term><term>Biosynthèse</term><term>Voie nigrostriatale</term><term>Tyrosine 3-monooxygenase</term><term>Coordination sensorimotrice</term><term>Ataxie télangiectasie</term><term>Posture</term><term>Cervelet</term><term>Parkinson maladie</term><term>Souris</term><term>Animal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ataxia-telangiectasia (A-T) is a genetic disease, associated with progressive motor impairment and a lack of functional ATM protein. It has been reported that immunoreactive tyrosine hydroxylase and dopamine transporter are reduced in an Atm<sup>-/-</sup> mouse model of A-T. These observations led to a hypothesis that A-T is associated with loss of nigrostriatal dopamine and prompted the launch of clinical trials to evaluate a therapeutic utility of the anti-parkinsonian drug, L-DOPA. To test for dopamine depletion more directly, we measured regional levels of monoamines and their metabolites in the Atm<sup>-/-</sup>mouse brain. We also measured levels of NAD<sup>+</sup>, a cofactor for dopamine biosynthesis and substrate of the DNA damage surveillance enzyme, poly(ADP-ribose) polymerase (PARP). Constitutive activation of PARP has been posited to cause NAD<sup>+</sup> depletion. We observed no reduction in monoamine transmitters and no depletion of NAD<sup>+</sup>, or other high energy phosphate donors in the adult Atm<sup>-/-</sup> cerebellum, striatum, or ventral mesencephalon. However, our studies did reveal a progressive sensorimotor impairment in Atm<sup>-/-</sup>mice that may serve as a relevant proxy for progressive neurological impairment in the human disease. Our results call into question the involvement of dopamine in A-T and the therapeutic strategy of enhancing dopaminergic function with L-DOPA.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>88</s2></fA05><fA06><s2>6</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Progressive sensorimotor impairment is not associated with reduced dopamine and high energy phosphate donors in a model of ataxia-telangiectasia</s1></fA08><fA11 i1="01" i2="1"><s1>MOUNT (Howard T. J.)</s1></fA11><fA11 i1="02" i2="1"><s1>MARTEL (Jean-Claude)</s1></fA11><fA11 i1="03" i2="1"><s1>FLUIT (Paul)</s1></fA11><fA11 i1="04" i2="1"><s1>YINGJI WU</s1></fA11><fA11 i1="05" i2="1"><s1>GALLO-HENDRIKX (Eleanor)</s1></fA11><fA11 i1="06" i2="1"><s1>COSI (Cristina)</s1></fA11><fA11 i1="07" i2="1"><s1>MARIEN (Marc R.)</s1></fA11><fA14 i1="01"><s1>Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Division of Neurology, Department of Medicine, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ></fA14><fA14 i1="03"><s1>Institut de Reclterche Pierre Fabre</s1><s2>Castres</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></fA14><fA20><s1>1449-1454</s1></fA20><fA21><s1>2004</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4037</s2><s5>354000111456470160</s5></fA43><fA44><s0>0000</s0><s1>© 2004 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>32 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>04-0345628</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurochemistry</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Ataxia-telangiectasia (A-T) is a genetic disease, associated with progressive motor impairment and a lack of functional ATM protein. It has been reported that immunoreactive tyrosine hydroxylase and dopamine transporter are reduced in an Atm<sup>-/-</sup> mouse model of A-T. These observations led to a hypothesis that A-T is associated with loss of nigrostriatal dopamine and prompted the launch of clinical trials to evaluate a therapeutic utility of the anti-parkinsonian drug, L-DOPA. To test for dopamine depletion more directly, we measured regional levels of monoamines and their metabolites in the Atm<sup>-/-</sup>mouse brain. We also measured levels of NAD<sup>+</sup>, a cofactor for dopamine biosynthesis and substrate of the DNA damage surveillance enzyme, poly(ADP-ribose) polymerase (PARP). Constitutive activation of PARP has been posited to cause NAD<sup>+</sup> depletion. We observed no reduction in monoamine transmitters and no depletion of NAD<sup>+</sup>, or other high energy phosphate donors in the adult Atm<sup>-/-</sup> cerebellum, striatum, or ventral mesencephalon. However, our studies did reveal a progressive sensorimotor impairment in Atm<sup>-/-</sup>mice that may serve as a relevant proxy for progressive neurological impairment in the human disease. Our results call into question the involvement of dopamine in A-T and the therapeutic strategy of enhancing dopaminergic function with L-DOPA.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A01</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Dopamina</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Déplétion</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Depletion</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Depleción</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Biosynthèse</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Biosynthesis</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Biosíntesis</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Voie nigrostriatale</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Nigrostriatal pathway</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Vía nigroestriatal</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>NAD<sup>+</sup> ADP-ribosyltransferase</s0><s2>NK</s2><s2>FE</s2><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>NAD<sup>+</sup> ADP-ribosyltransferase</s0><s2>NK</s2><s2>FE</s2><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>NAD<sup>+</sup> ADP-ribosyltransferase</s0><s2>NK</s2><s2>FE</s2><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Tyrosine 3-monooxygenase</s0><s2>FE</s2><s5>06</s5><s6>Tyrosine «3»-monooxygenase</s6></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Tyrosine 3-monooxygenase</s0><s2>FE</s2><s5>06</s5><s6>Tyrosine «3»-monooxygenase</s6></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Tyrosine 3-monooxygenase</s0><s2>FE</s2><s5>06</s5><s6>Tyrosine «3»-monooxygenase</s6></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Coordination sensorimotrice</s0><s5>08</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Sensorimotor coordination</s0><s5>08</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Coordinación sensoriomotora</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Ataxie télangiectasie</s0><s5>09</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Ataxia telangiectasia</s0><s5>09</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Ataxia telangiectasia</s0><s5>09</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Posture</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Posture</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Postura</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Cervelet</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Cerebellum</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Cerebelo</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>12</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Parkinson disease</s0><s5>12</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s5>12</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Souris</s0><s5>54</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Mouse</s0><s5>54</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Ratón</s0><s5>54</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Animal</s0><s5>69</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Animal</s0><s5>69</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Animal</s0><s5>69</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>NAD<sup>+</sup></s0><s4>CD</s4><s5>96</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>NAD<sup>+</sup></s0><s4>CD</s4><s5>96</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Pentosyltransferases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Pentosyltransferases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Pentosyltransferases</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Glycosyltransferases</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Glycosyltransferases</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Glycosyltransferases</s0><s2>FE</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Transferases</s0><s2>FE</s2></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Transferases</s0><s2>FE</s2></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Transferases</s0><s2>FE</s2></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Enzima</s0><s2>FE</s2></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Neurotransmetteur</s0><s5>20</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Neurotransmitter</s0><s5>20</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Neurotransmisor</s0><s5>20</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Catécholamine</s0><s5>21</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Catecholamine</s0><s5>21</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Catecolamina</s0><s5>21</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>38</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>38</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>38</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Appareil circulatoire pathologie</s0><s5>39</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Cardiovascular disease</s0><s5>39</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Aparato circulatorio patología</s0><s5>39</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Vaisseau sanguin pathologie</s0><s5>40</s5></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Vascular disease</s0><s5>40</s5></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Vaso sanguíneo patología</s0><s5>40</s5></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Oeil pathologie</s0><s5>41</s5></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Eye disease</s0><s5>41</s5></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Ojo patología</s0><s5>41</s5></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Peau pathologie</s0><s5>42</s5></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Skin disease</s0><s5>42</s5></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Piel patología</s0><s5>42</s5></fC07><fC07 i1="13" i2="X" l="FRE"><s0>Immunopathologie</s0><s5>43</s5></fC07><fC07 i1="13" i2="X" l="ENG"><s0>Immunopathology</s0><s5>43</s5></fC07><fC07 i1="13" i2="X" l="SPA"><s0>Inmunopatología</s0><s5>43</s5></fC07><fC07 i1="14" i2="X" l="FRE"><s0>Maladie héréditaire</s0><s5>44</s5></fC07><fC07 i1="14" i2="X" l="ENG"><s0>Genetic disease</s0><s5>44</s5></fC07><fC07 i1="14" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0><s5>44</s5></fC07><fC07 i1="15" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>46</s5></fC07><fC07 i1="15" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>46</s5></fC07><fC07 i1="15" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>46</s5></fC07><fC07 i1="16" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>47</s5></fC07><fC07 i1="16" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>47</s5></fC07><fC07 i1="16" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>47</s5></fC07><fC07 i1="17" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>48</s5></fC07><fC07 i1="17" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>48</s5></fC07><fC07 i1="17" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>48</s5></fC07><fC07 i1="18" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>49</s5></fC07><fC07 i1="18" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>49</s5></fC07><fC07 i1="18" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>49</s5></fC07><fC07 i1="19" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="19" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="19" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="20" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="20" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="20" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="21" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="21" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="21" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>201</s1></fN21></pA></standard><server><NO>PASCAL 04-0345628 INIST</NO><ET>Progressive sensorimotor impairment is not associated with reduced dopamine and high energy phosphate donors in a model of ataxia-telangiectasia</ET><AU>MOUNT (Howard T. J.); MARTEL (Jean-Claude); FLUIT (Paul); YINGJI WU; GALLO-HENDRIKX (Eleanor); COSI (Cristina); MARIEN (Marc R.)</AU><AF>Centre for Research in Neurodegenerative Diseases, Department of Medicine, University of Toronto/Toronto, Ontario/Canada (1 aut., 3 aut., 4 aut., 5 aut.); Division of Neurology, Department of Medicine, University of Toronto/Toronto, Ontario/Canada (1 aut.); Institut de Reclterche Pierre Fabre/Castres/France (2 aut., 6 aut., 7 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2004; Vol. 88; No. 6; Pp. 1449-1454; Bibl. 32 ref.</SO><LA>Anglais</LA><EA>Ataxia-telangiectasia (A-T) is a genetic disease, associated with progressive motor impairment and a lack of functional ATM protein. It has been reported that immunoreactive tyrosine hydroxylase and dopamine transporter are reduced in an Atm<sup>-/-</sup> mouse model of A-T. These observations led to a hypothesis that A-T is associated with loss of nigrostriatal dopamine and prompted the launch of clinical trials to evaluate a therapeutic utility of the anti-parkinsonian drug, L-DOPA. To test for dopamine depletion more directly, we measured regional levels of monoamines and their metabolites in the Atm<sup>-/-</sup>mouse brain. We also measured levels of NAD<sup>+</sup>, a cofactor for dopamine biosynthesis and substrate of the DNA damage surveillance enzyme, poly(ADP-ribose) polymerase (PARP). Constitutive activation of PARP has been posited to cause NAD<sup>+</sup> depletion. We observed no reduction in monoamine transmitters and no depletion of NAD<sup>+</sup>, or other high energy phosphate donors in the adult Atm<sup>-/-</sup> cerebellum, striatum, or ventral mesencephalon. However, our studies did reveal a progressive sensorimotor impairment in Atm<sup>-/-</sup>mice that may serve as a relevant proxy for progressive neurological impairment in the human disease. Our results call into question the involvement of dopamine in A-T and the therapeutic strategy of enhancing dopaminergic function with L-DOPA.</EA><CC>002B17G; 002B17A01</CC><FD>Dopamine; Déplétion; Biosynthèse; Voie nigrostriatale; NAD<sup>+</sup> ADP-ribosyltransferase; Tyrosine 3-monooxygenase; Coordination sensorimotrice; Ataxie télangiectasie; Posture; Cervelet; Parkinson maladie; Souris; Animal; NAD<sup>+</sup></FD><FG>Pentosyltransferases; Glycosyltransferases; Transferases; Enzyme; Oxidoreductases; Neurotransmetteur; Catécholamine; Système nerveux pathologie; Appareil circulatoire pathologie; Vaisseau sanguin pathologie; Oeil pathologie; Peau pathologie; Immunopathologie; Maladie héréditaire; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata</FG><ED>Dopamine; Depletion; Biosynthesis; Nigrostriatal pathway; NAD<sup>+</sup> ADP-ribosyltransferase; Tyrosine 3-monooxygenase; Sensorimotor coordination; Ataxia telangiectasia; Posture; Cerebellum; Parkinson disease; Mouse; Animal; NAD<sup>+</sup></ED><EG>Pentosyltransferases; Glycosyltransferases; Transferases; Enzyme; Oxidoreductases; Neurotransmitter; Catecholamine; Nervous system diseases; Cardiovascular disease; Vascular disease; Eye disease; Skin disease; Immunopathology; Genetic disease; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata</EG><SD>Dopamina; Depleción; Biosíntesis; Vía nigroestriatal; NAD<sup>+</sup> ADP-ribosyltransferase; Tyrosine 3-monooxygenase; Coordinación sensoriomotora; Ataxia telangiectasia; Postura; Cerebelo; Parkinson enfermedad; Ratón; Animal</SD><LO>INIST-4037.354000111456470160</LO><ID>04-0345628</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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