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 : 000141Expression 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 :
- Experimental neurology : (Print) [ 0014-4886 ] ; 2000.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme, Personne âgée.
English descriptors
- KwdEn :
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.
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<front><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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<fC03 i1="08" i2="X" l="ENG"><s0>Rat</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Rata</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Personne âgée</s0>
<s5>22</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Elderly</s0>
<s5>22</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Anciano</s0>
<s5>22</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Expression génique</s0>
<s5>23</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Gene expression</s0>
<s5>23</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Expresión genética</s0>
<s5>23</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Facteur croissance nerf</s0>
<s5>24</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Nerve growth factor</s0>
<s5>24</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Factor crecimiento nervio</s0>
<s5>24</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Aminoacide</s0>
<s5>25</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Aminoacid</s0>
<s5>25</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Aminoácido</s0>
<s5>25</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Cholérétique</s0>
<s5>26</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Choleretic</s0>
<s5>26</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Colerético</s0>
<s5>26</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>Hépatoprotecteur</s0>
<s5>27</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG"><s0>Hepatoprotector</s0>
<s5>27</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA"><s0>Hepatoprotector</s0>
<s5>27</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE"><s0>Site fixation</s0>
<s5>35</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG"><s0>Binding site</s0>
<s5>35</s5>
</fC03>
<fC03 i1="16" i2="X" l="SPA"><s0>Sitio fijación</s0>
<s5>35</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE"><s0>Récepteur trk</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>40</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fN21><s1>353</s1>
</fN21>
</pA>
</standard>
</inist>
</record>
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