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Expression of Trk isoforms in brain regions and in the striatum of patients with Alzheimer's disease

Identifieur interne : 000140 ( PascalFrancis/Curation ); précédent : 000139; suivant : 000141

Expression of Trk isoforms in brain regions and in the striatum of patients with Alzheimer's disease

Auteurs : Pierre Dubus [France] ; Baptiste Faucheux [France] ; Florence Boissiere [France] ; Alexis Groppi [France] ; Claude Vital [France] ; T. Anne Vital [France] ; Yves Agid [France] ; Etienne C. Hirsch [France] ; Jean Philippe Merlio [France]

Source :

RBID : Pascal:00-0529868

Descripteurs français

English descriptors

Abstract

The TrkAII tyrosine kinase receptor differs from the TrkAI isoform by an insertion of six amino acids in the extracellular domain. We used RT-PCR to determine their respective distribution in rat and human brain. Only trkAII transcripts were detected in 12 rat brain regions, while both trkAI and trkAII transcripts were detected in the cerebellum and pituitary gland. In human, both trkAI and trkAII transcripts were detected in the frontal, temporal, and occipital cortex and thalamus, while only trkAI transcripts were detected in the hippocampus and cerebellum. In the caudate and putamen, trkAII transcripts were exclusively detected. Thereafter, we studied the expression of TrkA isoforms in the striatum of five patients with Alzheimer's disease (AD), four patients with non-AD dementia, seven patients with Parkinson's disease, and six paired nondemented elderly control individuals. In controls and non-AD patients, a constant expression of trkAII transcripts was detected within all striatum parts. In AD patients, a heterogeneous decrease in trkAII expression was observed in the caudate, putamen, and ventral striatum, resulting either in a drop of trkAII transcript levels or in a weak coamplification of trkAII and trkAI transcripts. The alteration of TrkAII gene expression paralleled those of choline acetyltransferase. Together with previous data, this suggests that the alteration of trk gene expression could contribute to a decrease in NGF binding sites and its protective effects on cholinergic neurons of AD patients.
pA  
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A02 01      @0 EXNEAC
A03   1    @0 Exp. neurol. : (Print)
A05       @2 165
A06       @2 2
A08 01  1  ENG  @1 Expression of Trk isoforms in brain regions and in the striatum of patients with Alzheimer's disease
A11 01  1    @1 DUBUS (Pierre)
A11 02  1    @1 FAUCHEUX (Baptiste)
A11 03  1    @1 BOISSIERE (Florence)
A11 04  1    @1 GROPPI (Alexis)
A11 05  1    @1 VITAL (Claude)
A11 06  1    @1 VITAL (T. Anne)
A11 07  1    @1 AGID (Yves)
A11 08  1    @1 HIRSCH (Etienne C.)
A11 09  1    @1 MERLIO (Jean Philippe)
A14 01      @1 Laboratoire d'Histologie-Embryologie, EA 2406 Université de Bordeaux 2, BP 8 @2 33076 Bordeaux @3 FRA @Z 1 aut. @Z 4 aut. @Z 9 aut.
A14 02      @1 INSERM U289, Hôpital de la Salpêtrière @2 75651 Paris @3 FRA @Z 2 aut. @Z 3 aut. @Z 7 aut. @Z 8 aut.
A14 03      @1 Service d'Anatomie Pathologique, Hôpital Pellegrin @2 33076 Bordeaux @3 FRA @Z 5 aut. @Z 6 aut.
A20       @1 285-294
A21       @1 2000
A23 01      @0 ENG
A43 01      @1 INIST @2 9181 @5 354000091146470090
A44       @0 0000 @1 © 2000 INIST-CNRS. All rights reserved.
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A60       @1 P
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A64 01  1    @0 Experimental neurology : (Print)
A66 01      @0 USA
C01 01    ENG  @0 The TrkAII tyrosine kinase receptor differs from the TrkAI isoform by an insertion of six amino acids in the extracellular domain. We used RT-PCR to determine their respective distribution in rat and human brain. Only trkAII transcripts were detected in 12 rat brain regions, while both trkAI and trkAII transcripts were detected in the cerebellum and pituitary gland. In human, both trkAI and trkAII transcripts were detected in the frontal, temporal, and occipital cortex and thalamus, while only trkAI transcripts were detected in the hippocampus and cerebellum. In the caudate and putamen, trkAII transcripts were exclusively detected. Thereafter, we studied the expression of TrkA isoforms in the striatum of five patients with Alzheimer's disease (AD), four patients with non-AD dementia, seven patients with Parkinson's disease, and six paired nondemented elderly control individuals. In controls and non-AD patients, a constant expression of trkAII transcripts was detected within all striatum parts. In AD patients, a heterogeneous decrease in trkAII expression was observed in the caudate, putamen, and ventral striatum, resulting either in a drop of trkAII transcript levels or in a weak coamplification of trkAII and trkAI transcripts. The alteration of TrkAII gene expression paralleled those of choline acetyltransferase. Together with previous data, this suggests that the alteration of trk gene expression could contribute to a decrease in NGF binding sites and its protective effects on cholinergic neurons of AD patients.
C02 01  X    @0 002B17G
C03 01  X  FRE  @0 Démence Alzheimer @5 01
C03 01  X  ENG  @0 Alzheimer disease @5 01
C03 01  X  SPA  @0 Demencia Alzheimer @5 01
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C03 02  X  ENG  @0 Parkinson disease @5 04
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C03 03  X  FRE  @0 Forme moléculaire @5 07
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C03 07  X  SPA  @0 Protein-tyrosine kinase @2 FE @5 19
C03 08  X  FRE  @0 Rat @5 20
C03 08  X  ENG  @0 Rat @5 20
C03 08  X  SPA  @0 Rata @5 20
C03 09  X  FRE  @0 Animal @5 21
C03 09  X  ENG  @0 Animal @5 21
C03 09  X  SPA  @0 Animal @5 21
C03 10  X  FRE  @0 Personne âgée @5 22
C03 10  X  ENG  @0 Elderly @5 22
C03 10  X  SPA  @0 Anciano @5 22
C03 11  X  FRE  @0 Expression génique @5 23
C03 11  X  ENG  @0 Gene expression @5 23
C03 11  X  SPA  @0 Expresión genética @5 23
C03 12  X  FRE  @0 Facteur croissance nerf @5 24
C03 12  X  ENG  @0 Nerve growth factor @5 24
C03 12  X  SPA  @0 Factor crecimiento nervio @5 24
C03 13  X  FRE  @0 Aminoacide @5 25
C03 13  X  ENG  @0 Aminoacid @5 25
C03 13  X  SPA  @0 Aminoácido @5 25
C03 14  X  FRE  @0 Cholérétique @5 26
C03 14  X  ENG  @0 Choleretic @5 26
C03 14  X  SPA  @0 Colerético @5 26
C03 15  X  FRE  @0 Hépatoprotecteur @5 27
C03 15  X  ENG  @0 Hepatoprotector @5 27
C03 15  X  SPA  @0 Hepatoprotector @5 27
C03 16  X  FRE  @0 Site fixation @5 35
C03 16  X  ENG  @0 Binding site @5 35
C03 16  X  SPA  @0 Sitio fijación @5 35
C03 17  X  FRE  @0 Récepteur trk @4 INC @5 86
C07 01  X  FRE  @0 Transferases @2 FE
C07 01  X  ENG  @0 Transferases @2 FE
C07 01  X  SPA  @0 Transferases @2 FE
C07 02  X  FRE  @0 Enzyme
C07 02  X  ENG  @0 Enzyme
C07 02  X  SPA  @0 Enzima
C07 03  X  FRE  @0 Rodentia @2 NS
C07 03  X  ENG  @0 Rodentia @2 NS
C07 03  X  SPA  @0 Rodentia @2 NS
C07 04  X  FRE  @0 Mammalia @2 NS
C07 04  X  ENG  @0 Mammalia @2 NS
C07 04  X  SPA  @0 Mammalia @2 NS
C07 05  X  FRE  @0 Vertebrata @2 NS
C07 05  X  ENG  @0 Vertebrata @2 NS
C07 05  X  SPA  @0 Vertebrata @2 NS
C07 06  X  FRE  @0 Encéphale pathologie @5 37
C07 06  X  ENG  @0 Cerebral disorder @5 37
C07 06  X  SPA  @0 Encéfalo patología @5 37
C07 07  X  FRE  @0 Système nerveux pathologie @5 38
C07 07  X  ENG  @0 Nervous system diseases @5 38
C07 07  X  SPA  @0 Sistema nervioso patología @5 38
C07 08  X  FRE  @0 Système nerveux central pathologie @5 39
C07 08  X  ENG  @0 Central nervous system disease @5 39
C07 08  X  SPA  @0 Sistema nervosio central patología @5 39
C07 09  X  FRE  @0 Maladie dégénérative @5 40
C07 09  X  ENG  @0 Degenerative disease @5 40
C07 09  X  SPA  @0 Enfermedad degenerativa @5 40
C07 10  X  FRE  @0 Extrapyramidal syndrome @5 41
C07 10  X  ENG  @0 Extrapyramidal syndrome @5 41
C07 10  X  SPA  @0 Extrapiramidal síndrome @5 41
N21       @1 353

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<term>Choleretic</term>
<term>Corpus striatum</term>
<term>Elderly</term>
<term>Gene expression</term>
<term>Hepatoprotector</term>
<term>Human</term>
<term>Localization</term>
<term>Molecular form</term>
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<term>Démence Alzheimer</term>
<term>Parkinson maladie</term>
<term>Forme moléculaire</term>
<term>Corps strié</term>
<term>Localisation</term>
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<term>Protein-tyrosine kinase</term>
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<term>Personne âgée</term>
<term>Expression génique</term>
<term>Facteur croissance nerf</term>
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<term>Site fixation</term>
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<div type="abstract" xml:lang="en">The TrkAII tyrosine kinase receptor differs from the TrkAI isoform by an insertion of six amino acids in the extracellular domain. We used RT-PCR to determine their respective distribution in rat and human brain. Only trkAII transcripts were detected in 12 rat brain regions, while both trkAI and trkAII transcripts were detected in the cerebellum and pituitary gland. In human, both trkAI and trkAII transcripts were detected in the frontal, temporal, and occipital cortex and thalamus, while only trkAI transcripts were detected in the hippocampus and cerebellum. In the caudate and putamen, trkAII transcripts were exclusively detected. Thereafter, we studied the expression of TrkA isoforms in the striatum of five patients with Alzheimer's disease (AD), four patients with non-AD dementia, seven patients with Parkinson's disease, and six paired nondemented elderly control individuals. In controls and non-AD patients, a constant expression of trkAII transcripts was detected within all striatum parts. In AD patients, a heterogeneous decrease in trkAII expression was observed in the caudate, putamen, and ventral striatum, resulting either in a drop of trkAII transcript levels or in a weak coamplification of trkAII and trkAI transcripts. The alteration of TrkAII gene expression paralleled those of choline acetyltransferase. Together with previous data, this suggests that the alteration of trk gene expression could contribute to a decrease in NGF binding sites and its protective effects on cholinergic neurons of AD patients.</div>
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<s0>The TrkAII tyrosine kinase receptor differs from the TrkAI isoform by an insertion of six amino acids in the extracellular domain. We used RT-PCR to determine their respective distribution in rat and human brain. Only trkAII transcripts were detected in 12 rat brain regions, while both trkAI and trkAII transcripts were detected in the cerebellum and pituitary gland. In human, both trkAI and trkAII transcripts were detected in the frontal, temporal, and occipital cortex and thalamus, while only trkAI transcripts were detected in the hippocampus and cerebellum. In the caudate and putamen, trkAII transcripts were exclusively detected. Thereafter, we studied the expression of TrkA isoforms in the striatum of five patients with Alzheimer's disease (AD), four patients with non-AD dementia, seven patients with Parkinson's disease, and six paired nondemented elderly control individuals. In controls and non-AD patients, a constant expression of trkAII transcripts was detected within all striatum parts. In AD patients, a heterogeneous decrease in trkAII expression was observed in the caudate, putamen, and ventral striatum, resulting either in a drop of trkAII transcript levels or in a weak coamplification of trkAII and trkAI transcripts. The alteration of TrkAII gene expression paralleled those of choline acetyltransferase. Together with previous data, this suggests that the alteration of trk gene expression could contribute to a decrease in NGF binding sites and its protective effects on cholinergic neurons of AD patients.</s0>
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<s0>Transferases</s0>
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<s0>Transferases</s0>
<s2>FE</s2>
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