ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000394

Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases

Identifieur interne : 000394 ( PascalFrancis/Corpus ); précédent : 000393; suivant : 000395

Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases

Auteurs : Mélanie Bousquet ; Claire Gibrat ; Mélissa Ouellet ; Claude Rouillard ; Frédéric Calon ; Francesca Cicchetti

Source :

Journal of neurochemistry [ 0022-3042 ] ; 2010.

RBID : Pascal:10-0434654

Descripteurs français

Pascal (Inist)
- Métabolisme, Encéphale, Transport biologique, Test clinique, Métabolite, Taurine, Cystéine, Phosphate, Maladie de Parkinson, Seuil détection, Détection seuil, Barrière hématoencéphalique, Perfusion, Souris.

English descriptors

KwdEn :
- Biological transport, Blood brain barrier, Clinical test, Cysteine, Detection threshold, Encephalon, Metabolism, Metabolite, Mouse, Parkinson disease, Perfusion, Phosphates, Taurine, Threshold detection.

Abstract

Cystamine has shown significant neuroprotective properties in preclinical studies of Parkinson's disease (PD) and Hunting-ton's disease (HD). Cysteamine, its FDA-approved reduced form, is scheduled to be tested for clinical efficacy in HD patients. Here, we studied the key cystamine metabolites, namely cysteamine, hypotaurine and taurine, as well as cysteine, in order to identify which one is more distinctively responsible for the neuroprotective action of cystamine. After a single administration of cystamine (10, 50 or 200 mg/kg), naive mice were perfused with phosphate-buffered saline (PBS) at 1, 3, 12, 24 or 48 h post-injection and brain and plasma samples were analyzed by two distinct HPLC methods. Although plasma levels remained under the detection threshold, significant increases in cysteamine brain levels were detected with the 50 and 200 mg/kg doses in mice perfused 1 and 3 h following cystamine injection. To further assess cysteamine as the candidate molecule for pre-clinical and clinical trials in PD, we evaluated its capacity to cross the blood brain barrier. Using an in situ cerebral perfusion technique, we determined that the brain transport coefficient (Clup) of cysteamine (259 μM) was 0.15 ± 0.02 μL/g/s and was increased up to 0.34 ± 0.07 μL/g/s when co-perfused in the presence of cysteine. Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 10-0434654 INIST
ET :	Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases
AU :	BOUSQUET (Mélanie); GIBRAT (Claire); OUELLET (Mélissa); ROUILLARD (Claude); CALON (Frédéric); CICCHETTI (Francesca)
AF :	Centre de Recherche du CHUL (CHUQ), Axe Neurosciences/Québec, Québec/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut.); Département de Psychiatrie et Neurosciences, Université Laval/Québec, Québec/Canada (4 aut., 6 aut.); Faculté de Pharmacie, Université Laval/Québec, Québec/Canada (1 aut., 3 aut., 5 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2010; Vol. 114; No. 6; Pp. 1651-1658; Bibl. 1 p.1/4
LA :	Anglais
EA :	Cystamine has shown significant neuroprotective properties in preclinical studies of Parkinson's disease (PD) and Hunting-ton's disease (HD). Cysteamine, its FDA-approved reduced form, is scheduled to be tested for clinical efficacy in HD patients. Here, we studied the key cystamine metabolites, namely cysteamine, hypotaurine and taurine, as well as cysteine, in order to identify which one is more distinctively responsible for the neuroprotective action of cystamine. After a single administration of cystamine (10, 50 or 200 mg/kg), naive mice were perfused with phosphate-buffered saline (PBS) at 1, 3, 12, 24 or 48 h post-injection and brain and plasma samples were analyzed by two distinct HPLC methods. Although plasma levels remained under the detection threshold, significant increases in cysteamine brain levels were detected with the 50 and 200 mg/kg doses in mice perfused 1 and 3 h following cystamine injection. To further assess cysteamine as the candidate molecule for pre-clinical and clinical trials in PD, we evaluated its capacity to cross the blood brain barrier. Using an in situ cerebral perfusion technique, we determined that the brain transport coefficient (Clup) of cysteamine (259 μM) was 0.15 ± 0.02 μL/g/s and was increased up to 0.34 ± 0.07 μL/g/s when co-perfused in the presence of cysteine. Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.
CC :	002B17G; 002B17A01
FD :	Métabolisme; Encéphale; Transport biologique; Test clinique; Métabolite; Taurine; Cystéine; Phosphate; Maladie de Parkinson; Seuil détection; Détection seuil; Barrière hématoencéphalique; Perfusion; Souris
FG :	Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux; Rodentia; Mammalia; Vertebrata
ED :	Metabolism; Encephalon; Biological transport; Clinical test; Metabolite; Taurine; Cysteine; Phosphates; Parkinson disease; Detection threshold; Threshold detection; Blood brain barrier; Perfusion; Mouse
EG :	Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Rodentia; Mammalia; Vertebrata
SD :	Metabolismo; Encéfalo; Transporte biológico; Prueba clínica; Metabolito; Taurina; Cisteína; Fosfato; Parkinson enfermedad; Umbral detección; Detección umbral; Barrera hematoencefálica; Perfusión; Ratón
LO :	INIST-4037.354000192648950110
ID :	10-0434654

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Le document en format XML

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<sZ>4 aut.</sZ>
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<series><title level="j" type="main">Journal of neurochemistry</title>
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<idno type="ISSN">0022-3042</idno>
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<term>Blood brain barrier</term>
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<term>Cysteine</term>
<term>Detection threshold</term>
<term>Encephalon</term>
<term>Metabolism</term>
<term>Metabolite</term>
<term>Mouse</term>
<term>Parkinson disease</term>
<term>Perfusion</term>
<term>Phosphates</term>
<term>Taurine</term>
<term>Threshold detection</term>
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<term>Encéphale</term>
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<term>Test clinique</term>
<term>Métabolite</term>
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<term>Cystéine</term>
<term>Phosphate</term>
<term>Maladie de Parkinson</term>
<term>Seuil détection</term>
<term>Détection seuil</term>
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<front><div type="abstract" xml:lang="en">Cystamine has shown significant neuroprotective properties in preclinical studies of Parkinson's disease (PD) and Hunting-ton's disease (HD). Cysteamine, its FDA-approved reduced form, is scheduled to be tested for clinical efficacy in HD patients. Here, we studied the key cystamine metabolites, namely cysteamine, hypotaurine and taurine, as well as cysteine, in order to identify which one is more distinctively responsible for the neuroprotective action of cystamine. After a single administration of cystamine (10, 50 or 200 mg/kg), naive mice were perfused with phosphate-buffered saline (PBS) at 1, 3, 12, 24 or 48 h post-injection and brain and plasma samples were analyzed by two distinct HPLC methods. Although plasma levels remained under the detection threshold, significant increases in cysteamine brain levels were detected with the 50 and 200 mg/kg doses in mice perfused 1 and 3 h following cystamine injection. To further assess cysteamine as the candidate molecule for pre-clinical and clinical trials in PD, we evaluated its capacity to cross the blood brain barrier. Using an in situ cerebral perfusion technique, we determined that the brain transport coefficient (Clup) of cysteamine (259 μM) was 0.15 ± 0.02 μL/g/s and was increased up to 0.34 ± 0.07 μL/g/s when co-perfused in the presence of cysteine. Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.</div>
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<server><NO>PASCAL 10-0434654 INIST</NO>
<ET>Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases</ET>
<AU>BOUSQUET (Mélanie); GIBRAT (Claire); OUELLET (Mélissa); ROUILLARD (Claude); CALON (Frédéric); CICCHETTI (Francesca)</AU>
<AF>Centre de Recherche du CHUL (CHUQ), Axe Neurosciences/Québec, Québec/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut.); Département de Psychiatrie et Neurosciences, Université Laval/Québec, Québec/Canada (4 aut., 6 aut.); Faculté de Pharmacie, Université Laval/Québec, Québec/Canada (1 aut., 3 aut., 5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Royaume-Uni; Da. 2010; Vol. 114; No. 6; Pp. 1651-1658; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>Cystamine has shown significant neuroprotective properties in preclinical studies of Parkinson's disease (PD) and Hunting-ton's disease (HD). Cysteamine, its FDA-approved reduced form, is scheduled to be tested for clinical efficacy in HD patients. Here, we studied the key cystamine metabolites, namely cysteamine, hypotaurine and taurine, as well as cysteine, in order to identify which one is more distinctively responsible for the neuroprotective action of cystamine. After a single administration of cystamine (10, 50 or 200 mg/kg), naive mice were perfused with phosphate-buffered saline (PBS) at 1, 3, 12, 24 or 48 h post-injection and brain and plasma samples were analyzed by two distinct HPLC methods. Although plasma levels remained under the detection threshold, significant increases in cysteamine brain levels were detected with the 50 and 200 mg/kg doses in mice perfused 1 and 3 h following cystamine injection. To further assess cysteamine as the candidate molecule for pre-clinical and clinical trials in PD, we evaluated its capacity to cross the blood brain barrier. Using an in situ cerebral perfusion technique, we determined that the brain transport coefficient (Clup) of cysteamine (259 μM) was 0.15 ± 0.02 μL/g/s and was increased up to 0.34 ± 0.07 μL/g/s when co-perfused in the presence of cysteine. Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.</EA>
<CC>002B17G; 002B17A01</CC>
<FD>Métabolisme; Encéphale; Transport biologique; Test clinique; Métabolite; Taurine; Cystéine; Phosphate; Maladie de Parkinson; Seuil détection; Détection seuil; Barrière hématoencéphalique; Perfusion; Souris</FD>
<FG>Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central; Pathologie du système nerveux; Rodentia; Mammalia; Vertebrata</FG>
<ED>Metabolism; Encephalon; Biological transport; Clinical test; Metabolite; Taurine; Cysteine; Phosphates; Parkinson disease; Detection threshold; Threshold detection; Blood brain barrier; Perfusion; Mouse</ED>
<EG>Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Rodentia; Mammalia; Vertebrata</EG>
<SD>Metabolismo; Encéfalo; Transporte biológico; Prueba clínica; Metabolito; Taurina; Cisteína; Fosfato; Parkinson enfermedad; Umbral detección; Detección umbral; Barrera hematoencefálica; Perfusión; Ratón</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)

Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases

Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases

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