Movement Disorders (revue)

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Selective loss of striatal preprotachykinin neurons in a phenocopy of Huntington's disease

Identifieur interne : 002791 ( PascalFrancis/Corpus ); précédent : 002790; suivant : 002792

Selective loss of striatal preprotachykinin neurons in a phenocopy of Huntington's disease

Auteurs : Eric K. Richfield ; Jean-Paul Vonsattel ; Marcy E. Macdonald ; ZHIQIANG SUN ; Yun-Ping P. Deng ; Anton Reiner

Source :

RBID : Pascal:02-0309341

Descripteurs français

English descriptors

Abstract

Phenocopies of Huntington's disease (HD) are individuals with a family history, clinical symptoms, and occasionally pathological evidence of HD but without an expanded CAG repeat within the HD gene. We report on an HD phenocopy with selective loss of preprotachykinin (PPT) neurons, dysfunction of surviving PPT neurons, preservation of preproenkephalin (PPE) neurons within the striatum, and greater loss of immunohistochemical staining for substance P in terminals of striatal neurons projecting to the substantia nigra, than in those projecting to the internal pallidal segment. This case demonstrates the existence of one type of striatal lesion that may produce a clinical picture similar to HD, and raises the possibility of a rare hereditary disease that mimics HD.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03   1    @0 Mov. disord.
A05       @2 17
A06       @2 2
A08 01  1  ENG  @1 Selective loss of striatal preprotachykinin neurons in a phenocopy of Huntington's disease
A11 01  1    @1 RICHFIELD (Eric K.)
A11 02  1    @1 VONSATTEL (Jean-Paul)
A11 03  1    @1 MACDONALD (Marcy E.)
A11 04  1    @1 ZHIQIANG SUN
A11 05  1    @1 DENG (Yun-Ping P.)
A11 06  1    @1 REINER (Anton)
A14 01      @1 Department of Pathology and Laboratory Medicine and Center for Aging and Developmental Biology, University of Rochester School of Medicine and Dentistry @2 Rochester, New York @3 USA @Z 1 aut.
A14 02      @1 Laboratory for Molecular Neuropathology, Massachusetts General Hospital @2 Charlestown, Massachusetts @3 USA @Z 2 aut.
A14 03      @1 Molecular Neurogenetics Unit, Massachusetts General Hospital @2 Charlestown, Massachusetts @3 USA @Z 3 aut.
A14 04      @1 Department of Anatomy and Neurobiology, University of Tennessee, Memphis @2 Memphis, Tennessee @3 USA @Z 4 aut. @Z 5 aut. @Z 6 aut.
A20       @1 327-332
A21       @1 2002
A23 01      @0 ENG
A43 01      @1 INIST @2 20953 @5 354000100907450140
A44       @0 0000 @1 © 2002 INIST-CNRS. All rights reserved.
A45       @0 28 ref.
A47 01  1    @0 02-0309341
A60       @1 P
A61       @0 A
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C01 01    ENG  @0 Phenocopies of Huntington's disease (HD) are individuals with a family history, clinical symptoms, and occasionally pathological evidence of HD but without an expanded CAG repeat within the HD gene. We report on an HD phenocopy with selective loss of preprotachykinin (PPT) neurons, dysfunction of surviving PPT neurons, preservation of preproenkephalin (PPE) neurons within the striatum, and greater loss of immunohistochemical staining for substance P in terminals of striatal neurons projecting to the substantia nigra, than in those projecting to the internal pallidal segment. This case demonstrates the existence of one type of striatal lesion that may produce a clinical picture similar to HD, and raises the possibility of a rare hereditary disease that mimics HD.
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C03 01  X  SPA  @0 Corea Huntington @5 01
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C03 02  X  ENG  @0 Immunohistochemistry @5 04
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C03 03  X  ENG  @0 Tachykinin @5 07
C03 03  X  SPA  @0 Taquikinina @5 07
C03 04  X  FRE  @0 Corps strié @5 10
C03 04  X  ENG  @0 Corpus striatum @5 10
C03 04  X  SPA  @0 Cuerpo estriado @5 10
C03 05  X  FRE  @0 Perte @5 13
C03 05  X  ENG  @0 Loss @5 13
C03 05  X  SPA  @0 Pérdida @5 13
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C03 06  X  SPA  @0 Neurona @5 14
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C07 01  X  FRE  @0 Système nerveux pathologie @5 37
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C07 01  X  SPA  @0 Sistema nervioso patología @5 37
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C07 03  X  SPA  @0 Encéfalo patología @5 39
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C07 04  X  ENG  @0 Extrapyramidal syndrome @5 40
C07 04  X  SPA  @0 Extrapiramidal síndrome @5 40
C07 05  X  FRE  @0 Maladie dégénérative @5 41
C07 05  X  ENG  @0 Degenerative disease @5 41
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C07 08  X  FRE  @0 Hormone peptide @5 53
C07 08  X  ENG  @0 Peptide hormone @5 53
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N21       @1 175
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Format Inist (serveur)

NO : PASCAL 02-0309341 INIST
ET : Selective loss of striatal preprotachykinin neurons in a phenocopy of Huntington's disease
AU : RICHFIELD (Eric K.); VONSATTEL (Jean-Paul); MACDONALD (Marcy E.); ZHIQIANG SUN; DENG (Yun-Ping P.); REINER (Anton)
AF : Department of Pathology and Laboratory Medicine and Center for Aging and Developmental Biology, University of Rochester School of Medicine and Dentistry/Rochester, New York/Etats-Unis (1 aut.); Laboratory for Molecular Neuropathology, Massachusetts General Hospital/Charlestown, Massachusetts/Etats-Unis (2 aut.); Molecular Neurogenetics Unit, Massachusetts General Hospital/Charlestown, Massachusetts/Etats-Unis (3 aut.); Department of Anatomy and Neurobiology, University of Tennessee, Memphis/Memphis, Tennessee/Etats-Unis (4 aut., 5 aut., 6 aut.)
DT : Publication en série; Niveau analytique
SO : Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2002; Vol. 17; No. 2; Pp. 327-332; Bibl. 28 ref.
LA : Anglais
EA : Phenocopies of Huntington's disease (HD) are individuals with a family history, clinical symptoms, and occasionally pathological evidence of HD but without an expanded CAG repeat within the HD gene. We report on an HD phenocopy with selective loss of preprotachykinin (PPT) neurons, dysfunction of surviving PPT neurons, preservation of preproenkephalin (PPE) neurons within the striatum, and greater loss of immunohistochemical staining for substance P in terminals of striatal neurons projecting to the substantia nigra, than in those projecting to the internal pallidal segment. This case demonstrates the existence of one type of striatal lesion that may produce a clinical picture similar to HD, and raises the possibility of a rare hereditary disease that mimics HD.
CC : 002B17G
FD : Chorée Huntington; Immunohistochimie; Tachykinine; Corps strié; Perte; Neurone; Substance P; Physiopathologie; Homme; Préprotachykinine
FG : Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Maladie héréditaire; Anatomopathologie; Hormone peptide; Encéphale
ED : Huntington disease; Immunohistochemistry; Tachykinin; Corpus striatum; Loss; Neuron; Substance P; Pathophysiology; Human
EG : Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Pathology; Peptide hormone; Brain (vertebrata)
SD : Corea Huntington; Inmunohistoquímica; Taquikinina; Cuerpo estriado; Pérdida; Neurona; Substancia P; Fisiopatología; Hombre
LO : INIST-20953.354000100907450140
ID : 02-0309341

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Pascal:02-0309341

Le document en format XML

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<div type="abstract" xml:lang="en">Phenocopies of Huntington's disease (HD) are individuals with a family history, clinical symptoms, and occasionally pathological evidence of HD but without an expanded CAG repeat within the HD gene. We report on an HD phenocopy with selective loss of preprotachykinin (PPT) neurons, dysfunction of surviving PPT neurons, preservation of preproenkephalin (PPE) neurons within the striatum, and greater loss of immunohistochemical staining for substance P in terminals of striatal neurons projecting to the substantia nigra, than in those projecting to the internal pallidal segment. This case demonstrates the existence of one type of striatal lesion that may produce a clinical picture similar to HD, and raises the possibility of a rare hereditary disease that mimics HD.</div>
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<fC03 i1="04" i2="X" l="SPA">
<s0>Cuerpo estriado</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Perte</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Loss</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Pérdida</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Neurone</s0>
<s5>14</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Neuron</s0>
<s5>14</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Neurona</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Substance P</s0>
<s5>16</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Substance P</s0>
<s5>16</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
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<s5>16</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Physiopathologie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
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<s5>17</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Fisiopatología</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Préprotachykinine</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Maladie héréditaire</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Genetic disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Enfermedad hereditaria</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Anatomopathologie</s0>
<s5>45</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Pathology</s0>
<s5>45</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Anatomía patológica</s0>
<s5>45</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Hormone peptide</s0>
<s5>53</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Peptide hormone</s0>
<s5>53</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Hormona péptido</s0>
<s5>53</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Encéphale</s0>
<s5>61</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Brain (vertebrata)</s0>
<s5>61</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Encéfalo</s0>
<s5>61</s5>
</fC07>
<fN21>
<s1>175</s1>
</fN21>
<fN82>
<s1>PSI</s1>
</fN82>
</pA>
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<server>
<NO>PASCAL 02-0309341 INIST</NO>
<ET>Selective loss of striatal preprotachykinin neurons in a phenocopy of Huntington's disease</ET>
<AU>RICHFIELD (Eric K.); VONSATTEL (Jean-Paul); MACDONALD (Marcy E.); ZHIQIANG SUN; DENG (Yun-Ping P.); REINER (Anton)</AU>
<AF>Department of Pathology and Laboratory Medicine and Center for Aging and Developmental Biology, University of Rochester School of Medicine and Dentistry/Rochester, New York/Etats-Unis (1 aut.); Laboratory for Molecular Neuropathology, Massachusetts General Hospital/Charlestown, Massachusetts/Etats-Unis (2 aut.); Molecular Neurogenetics Unit, Massachusetts General Hospital/Charlestown, Massachusetts/Etats-Unis (3 aut.); Department of Anatomy and Neurobiology, University of Tennessee, Memphis/Memphis, Tennessee/Etats-Unis (4 aut., 5 aut., 6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2002; Vol. 17; No. 2; Pp. 327-332; Bibl. 28 ref.</SO>
<LA>Anglais</LA>
<EA>Phenocopies of Huntington's disease (HD) are individuals with a family history, clinical symptoms, and occasionally pathological evidence of HD but without an expanded CAG repeat within the HD gene. We report on an HD phenocopy with selective loss of preprotachykinin (PPT) neurons, dysfunction of surviving PPT neurons, preservation of preproenkephalin (PPE) neurons within the striatum, and greater loss of immunohistochemical staining for substance P in terminals of striatal neurons projecting to the substantia nigra, than in those projecting to the internal pallidal segment. This case demonstrates the existence of one type of striatal lesion that may produce a clinical picture similar to HD, and raises the possibility of a rare hereditary disease that mimics HD.</EA>
<CC>002B17G</CC>
<FD>Chorée Huntington; Immunohistochimie; Tachykinine; Corps strié; Perte; Neurone; Substance P; Physiopathologie; Homme; Préprotachykinine</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Maladie héréditaire; Anatomopathologie; Hormone peptide; Encéphale</FG>
<ED>Huntington disease; Immunohistochemistry; Tachykinin; Corpus striatum; Loss; Neuron; Substance P; Pathophysiology; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Pathology; Peptide hormone; Brain (vertebrata)</EG>
<SD>Corea Huntington; Inmunohistoquímica; Taquikinina; Cuerpo estriado; Pérdida; Neurona; Substancia P; Fisiopatología; Hombre</SD>
<LO>INIST-20953.354000100907450140</LO>
<ID>02-0309341</ID>
</server>
</inist>
</record>

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