MovDisordV3, PascalFrancis, Checkpoint, bibRecord, 001B87

Characterization of nigrostriatal dysfunction in spinocerebellar ataxia 17

Identifieur interne : 001B87 ( PascalFrancis/Checkpoint ); précédent : 001B86; suivant : 001B88

Characterization of nigrostriatal dysfunction in spinocerebellar ataxia 17

Auteurs : Elena Salvatore [Italie] ; Andrea Varrone [Italie] ; Valeria Sansone [Italie] ; Maria Nolano [Italie] ; Amalia C. Bruni [Italie] ; Anna De Rosa [Italie] ; Lucio Santoro [Italie] ; Sabina Pappata [Italie] ; Alessandro Filla [Italie] ; Giuseppe De Michele [Italie]

Source :

Movement disorders [ 0885-3185 ] ; 2006.

RBID : Pascal:06-0352389

Descripteurs français

Pascal (Inist)
- Système nerveux pathologie, Trouble fonctionnel, Ataxie spinocérébelleuse, Tomoscintigraphie émission monophotonique, Photon, Voie nigrostriatale, Voie dopaminergique.

English descriptors

KwdEn :
- Dopaminergic pathway, Dysfunction, Nervous system diseases, Nigrostriatal pathway, Photon, Single photon emission tomography, Spinocerebellar ataxia.

Abstract

Extrapyramidal signs are a main feature of spinocerebellar ataxia 17 (SCA17). However, the extent of dopaminergic dysfunction and its correlation with parkinsonian signs are not fully understood. In order to define this, we investigated five subjects from three different families with a pathological CAG/CAA expansion in the TATA-binding protein gene (SCA17), ranging from asymptomatic carrier to patient with advanced disease, by FP-CIT SPECT. Nigrostriatal dysfunction was present in patients manifesting a fully developed phenotype but not in preclinical and early stages. Dopamine transporter reduction was symmetrical and uniform in caudate and putamen and it correlated with the clinical severity of ataxia.

Affiliations:

Italie

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Extrapyramidal signs are a main feature of spinocerebellar ataxia 17 (SCA17). However, the extent of dopaminergic dysfunction and its correlation with parkinsonian signs are not fully understood. In order to define this, we investigated five subjects from three different families with a pathological CAG/CAA expansion in the TATA-binding protein gene (SCA17), ranging from asymptomatic carrier to patient with advanced disease, by FP-CIT SPECT. Nigrostriatal dysfunction was present in patients manifesting a fully developed phenotype but not in preclinical and early stages. Dopamine transporter reduction was symmetrical and uniform in caudate and putamen and it correlated with the clinical severity of ataxia.</div>
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<fC03 i1="06" i2="X" l="SPA"><s0>Vía nigroestriatal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Voie dopaminergique</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Dopaminergic pathway</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Vía dopaminérgica</s0>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>41</s5>
</fC07>
<fN21><s1>233</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations><list><country><li>Italie</li>
</country>
</list>
<tree><country name="Italie"><noRegion><name sortKey="Salvatore, Elena" sort="Salvatore, Elena" uniqKey="Salvatore E" first="Elena" last="Salvatore">Elena Salvatore</name>
</noRegion>
<name sortKey="Bruni, Amalia C" sort="Bruni, Amalia C" uniqKey="Bruni A" first="Amalia C." last="Bruni">Amalia C. Bruni</name>
<name sortKey="De Michele, Giuseppe" sort="De Michele, Giuseppe" uniqKey="De Michele G" first="Giuseppe" last="De Michele">Giuseppe De Michele</name>
<name sortKey="De Rosa, Anna" sort="De Rosa, Anna" uniqKey="De Rosa A" first="Anna" last="De Rosa">Anna De Rosa</name>
<name sortKey="Filla, Alessandro" sort="Filla, Alessandro" uniqKey="Filla A" first="Alessandro" last="Filla">Alessandro Filla</name>
<name sortKey="Nolano, Maria" sort="Nolano, Maria" uniqKey="Nolano M" first="Maria" last="Nolano">Maria Nolano</name>
<name sortKey="Pappata, Sabina" sort="Pappata, Sabina" uniqKey="Pappata S" first="Sabina" last="Pappata">Sabina Pappata</name>
<name sortKey="Sansone, Valeria" sort="Sansone, Valeria" uniqKey="Sansone V" first="Valeria" last="Sansone">Valeria Sansone</name>
<name sortKey="Santoro, Lucio" sort="Santoro, Lucio" uniqKey="Santoro L" first="Lucio" last="Santoro">Lucio Santoro</name>
<name sortKey="Varrone, Andrea" sort="Varrone, Andrea" uniqKey="Varrone A" first="Andrea" last="Varrone">Andrea Varrone</name>
</country>
</tree>
</affiliations>
</record>

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	Movement Disorders (revue)
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Movement Disorders (revue)

Characterization of nigrostriatal dysfunction in spinocerebellar ataxia 17

Characterization of nigrostriatal dysfunction in spinocerebellar ataxia 17

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