ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000B63

Brain proteasomal function in sporadic Parkinson's disease and related disorders

Identifieur interne : 000B63 ( PascalFrancis/Corpus ); précédent : 000B62; suivant : 000B64

Brain proteasomal function in sporadic Parkinson's disease and related disorders

Auteurs : Yoshiaki Furukawa ; Sophie Vigouroux ; Henry Wong ; Mark Guttman ; Ali H. Rajput ; LEE ANG ; Marièle Briand ; Stephen J. Kish ; Yves Briand

Source :

Annals of neurology [ 0364-5134 ] ; 2002.

RBID : Pascal:02-0447146

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Sporadique, Multicatalytic endopeptidase complex, Encéphale, Anatomopathologie, Exploration, Autopsie, Homme.

English descriptors

KwdEn :
- Autopsy, Brain (vertebrata), Exploration, Human, Multicatalytic endopeptidase complex, Parkinson disease, Pathology, Sporadic.

Abstract

Because genetic defects relating to the ubiquitin-proteasome system were reported in familial parkinsonism, we evaluated proteasomal function in autopsied brains with sporadic Parkinson's disease. We found that proteasome peptidase activities in a fraction specific to the proteasome were preserved in five brain areas (including the striatum) of Parkinson's disease where neuronal loss is not observed. Striatal protein levels of two proteasome subunits were normal in Parkinson's disease but reduced mildly in disease controls (multiple system atrophy). Our brain data suggest that a systemic, global disturbance in the catalytic activity and degradation ability of the proteasome itself is unlikely to explain the cause of Parkinson's disease.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A14	`04`			`@1 Division of Neurology, University of Saskatchewan @2 Saskatoon, Saskatchewan @3 CAN @Z 5 aut.`
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Format Inist (serveur)

NO :	PASCAL 02-0447146 INIST
ET :	Brain proteasomal function in sporadic Parkinson's disease and related disorders
AU :	FURUKAWA (Yoshiaki); VIGOUROUX (Sophie); WONG (Henry); GUTTMAN (Mark); RAJPUT (Ali H.); LEE ANG; BRIAND (Marièle); KISH (Stephen J.); BRIAND (Yves)
AF :	Movement Disorders Research Laboratory, Centre for Addiction and Mental Health-Clarke Division/Toronto, Ontario/Canada (1 aut., 3 aut.); Laboratoire de Biochimie Appliquée, Université Blaise Pascal/Clermont Ferrand/France (2 aut., 7 aut., 9 aut.); Human Neurochemical Pathology Laboratory, Centre for Addiction and Mental Health-Clarke Division/Toronto, Ontario/Canada (4 aut., 8 aut.); Division of Neurology, University of Saskatchewan/Saskatoon, Saskatchewan/Canada (5 aut.); Department of Pathology, University of Western Ontario/London, Ontario/Canada (6 aut.)
DT :	Publication en série; Courte communication, note brève; Niveau analytique
SO :	Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2002; Vol. 51; No. 6; Pp. 779-782; Bibl. 20 ref.
LA :	Anglais
EA :	Because genetic defects relating to the ubiquitin-proteasome system were reported in familial parkinsonism, we evaluated proteasomal function in autopsied brains with sporadic Parkinson's disease. We found that proteasome peptidase activities in a fraction specific to the proteasome were preserved in five brain areas (including the striatum) of Parkinson's disease where neuronal loss is not observed. Striatal protein levels of two proteasome subunits were normal in Parkinson's disease but reduced mildly in disease controls (multiple system atrophy). Our brain data suggest that a systemic, global disturbance in the catalytic activity and degradation ability of the proteasome itself is unlikely to explain the cause of Parkinson's disease.
CC :	002B17G
FD :	Parkinson maladie; Sporadique; Multicatalytic endopeptidase complex; Encéphale; Anatomopathologie; Exploration; Autopsie; Homme
FG :	Peptidases; Hydrolases; Enzyme; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central
ED :	Parkinson disease; Sporadic; Multicatalytic endopeptidase complex; Brain (vertebrata); Pathology; Exploration; Autopsy; Human
EG :	Peptidases; Hydrolases; Enzyme; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system
SD :	Parkinson enfermedad; Esporádico; Multicatalytic endopeptidase complex; Encéfalo; Anatomía patológica; Exploración; Autopsia; Hombre
LO :	INIST-16555.354000108653100190
ID :	02-0447146

Links to Exploration step

Pascal:02-0447146

Le document en format XML

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<front><div type="abstract" xml:lang="en">Because genetic defects relating to the ubiquitin-proteasome system were reported in familial parkinsonism, we evaluated proteasomal function in autopsied brains with sporadic Parkinson's disease. We found that proteasome peptidase activities in a fraction specific to the proteasome were preserved in five brain areas (including the striatum) of Parkinson's disease where neuronal loss is not observed. Striatal protein levels of two proteasome subunits were normal in Parkinson's disease but reduced mildly in disease controls (multiple system atrophy). Our brain data suggest that a systemic, global disturbance in the catalytic activity and degradation ability of the proteasome itself is unlikely to explain the cause of Parkinson's disease.</div>
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<fA14 i1="03"><s1>Human Neurochemical Pathology Laboratory, Centre for Addiction and Mental Health-Clarke Division</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>4 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Division of Neurology, University of Saskatchewan</s1>
<s2>Saskatoon, Saskatchewan</s2>
<s3>CAN</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Pathology, University of Western Ontario</s1>
<s2>London, Ontario</s2>
<s3>CAN</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20><s1>779-782</s1>
</fA20>
<fA21><s1>2002</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
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<fC01 i1="01" l="ENG"><s0>Because genetic defects relating to the ubiquitin-proteasome system were reported in familial parkinsonism, we evaluated proteasomal function in autopsied brains with sporadic Parkinson's disease. We found that proteasome peptidase activities in a fraction specific to the proteasome were preserved in five brain areas (including the striatum) of Parkinson's disease where neuronal loss is not observed. Striatal protein levels of two proteasome subunits were normal in Parkinson's disease but reduced mildly in disease controls (multiple system atrophy). Our brain data suggest that a systemic, global disturbance in the catalytic activity and degradation ability of the proteasome itself is unlikely to explain the cause of Parkinson's disease.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
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</fC03>
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<s5>02</s5>
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</fC03>
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<s5>02</s5>
</fC03>
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<s5>04</s5>
</fC03>
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<fC03 i1="03" i2="X" l="SPA"><s0>Multicatalytic endopeptidase complex</s0>
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<s5>04</s5>
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<s5>10</s5>
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<fC03 i1="05" i2="X" l="ENG"><s0>Pathology</s0>
<s5>10</s5>
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<s5>10</s5>
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<fC03 i1="06" i2="X" l="ENG"><s0>Exploration</s0>
<s5>17</s5>
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<s5>18</s5>
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<s5>20</s5>
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<s5>20</s5>
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<s5>20</s5>
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<s2>FE</s2>
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<s2>FE</s2>
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<s2>FE</s2>
</fC07>
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<s2>FE</s2>
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<s2>FE</s2>
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<s2>FE</s2>
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</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>53</s5>
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<s5>53</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>53</s5>
</fC07>
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<server><NO>PASCAL 02-0447146 INIST</NO>
<ET>Brain proteasomal function in sporadic Parkinson's disease and related disorders</ET>
<AU>FURUKAWA (Yoshiaki); VIGOUROUX (Sophie); WONG (Henry); GUTTMAN (Mark); RAJPUT (Ali H.); LEE ANG; BRIAND (Marièle); KISH (Stephen J.); BRIAND (Yves)</AU>
<AF>Movement Disorders Research Laboratory, Centre for Addiction and Mental Health-Clarke Division/Toronto, Ontario/Canada (1 aut., 3 aut.); Laboratoire de Biochimie Appliquée, Université Blaise Pascal/Clermont Ferrand/France (2 aut., 7 aut., 9 aut.); Human Neurochemical Pathology Laboratory, Centre for Addiction and Mental Health-Clarke Division/Toronto, Ontario/Canada (4 aut., 8 aut.); Division of Neurology, University of Saskatchewan/Saskatoon, Saskatchewan/Canada (5 aut.); Department of Pathology, University of Western Ontario/London, Ontario/Canada (6 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2002; Vol. 51; No. 6; Pp. 779-782; Bibl. 20 ref.</SO>
<LA>Anglais</LA>
<EA>Because genetic defects relating to the ubiquitin-proteasome system were reported in familial parkinsonism, we evaluated proteasomal function in autopsied brains with sporadic Parkinson's disease. We found that proteasome peptidase activities in a fraction specific to the proteasome were preserved in five brain areas (including the striatum) of Parkinson's disease where neuronal loss is not observed. Striatal protein levels of two proteasome subunits were normal in Parkinson's disease but reduced mildly in disease controls (multiple system atrophy). Our brain data suggest that a systemic, global disturbance in the catalytic activity and degradation ability of the proteasome itself is unlikely to explain the cause of Parkinson's disease.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Sporadique; Multicatalytic endopeptidase complex; Encéphale; Anatomopathologie; Exploration; Autopsie; Homme</FD>
<FG>Peptidases; Hydrolases; Enzyme; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central</FG>
<ED>Parkinson disease; Sporadic; Multicatalytic endopeptidase complex; Brain (vertebrata); Pathology; Exploration; Autopsy; Human</ED>
<EG>Peptidases; Hydrolases; Enzyme; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system</EG>
<SD>Parkinson enfermedad; Esporádico; Multicatalytic endopeptidase complex; Encéfalo; Anatomía patológica; Exploración; Autopsia; Hombre</SD>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Brain proteasomal function in sporadic Parkinson's disease and related disorders

Brain proteasomal function in sporadic Parkinson's disease and related disorders

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