MovDisordV3, PascalFrancis, Corpus, bibRecord, 002936

Novel observations with FDOPA-PET imaging after early nigrostriatal damage

Identifieur interne : 002936 ( PascalFrancis/Corpus ); précédent : 002935; suivant : 002937

Novel observations with FDOPA-PET imaging after early nigrostriatal damage

Auteurs : R. E. Yee ; I. Irwin ; C. Milonas ; D. B. Stout ; S-C. Huang ; K. Shoghi-Jadid ; N. Satyamurthy ; L. E. Delanney ; D. M. Togasaki ; K. F. Farahani ; K. Delfani ; A. M. Janson ; M. E. Phelps ; J. W. Langston ; J. R. Barrio

Source :

Movement disorders [ 0885-3185 ] ; 2001.

RBID : Pascal:02-0049765

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Stade clinique, Asymptomatique, Tomographie émission positon, Fluorodopa(18F), Locus niger, Stéréologie, Neurone dopaminergique, Modèle animal, Evolution, Cinétique, Singe, Animal.

English descriptors

KwdEn :
- Animal, Animal model, Asymptomatic, Clinical stage, Dopaminergic neuron, Evolution, Fluorodopa(18F), Kinetics, Locus niger, Monkey, Parkinson disease, Positron emission tomography, Stereology.

Abstract

Striatal 6-[¹⁸F]fluoro-L-DOPA (FDOPA) kinetic rate constants were measured by positron emission tomography (PET) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated squirrel monkeys. After scanning, stereological counts of dopaminergic neurons were done in substantia nigra, and dopamine (DA) and metabolite concentrations were determined in the caudate, putamen, and substantia nigra. Graded doses of MPTP produced animals with mild to moderate reductions (10-35%) in dopaminergic neurons, where the percent of cell loss was proportional to the amount of MPTP given. Striatal DA and metabolite concentrations were relatively unchanged in animals given 1.0 and 1.5 mg/kg of MPTP, but were significantly reduced after 2.0 mg/kg of MPTP. All animals injected with a single dose of MPTP showed no overt signs of parkinsonism. In contrast, DA and metabolite concentrations in the substantia nigra were significantly reduced for all MPTP-treated animals. Reduction of dopaminergic indices in the substantia nigra did not parallel reductions in the striatum, indicating differential sensitivity of the nigrostriatal pathway to the neurotoxic effects of MPTP. The percent change in FDOPA uptake (Ki) and decarboyxlation (k₃) after MPTP showed significant positive correlations to striatal DA levels, but not to the number of dopaminergic neurons. This suggests that FDOPA is a good index of striatal DA levels.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 02-0049765 INIST
ET :	Novel observations with FDOPA-PET imaging after early nigrostriatal damage
AU :	YEE (R. E.); IRWIN (I.); MILONAS (C.); STOUT (D. B.); HUANG (S-C.); SHOGHI-JADID (K.); SATYAMURTHY (N.); DELANNEY (L. E.); TOGASAKI (D. M.); FARAHANI (K. F.); DELFANI (K.); JANSON (A. M.); PHELPS (M. E.); LANGSTON (J. W.); BARRIO (J. R.)
AF :	Department of Molecular and Medical Pharmacology, UCLA School of Medicine/Los Angeles, California/Etats-Unis (1 aut., 4 aut., 5 aut., 7 aut., 13 aut., 15 aut.); The Parkinson's Institute/Sunnyvale, California/Etats-Unis (2 aut., 8 aut., 9 aut., 14 aut.); Department of Neuroscience, Karolinska Institute/Stockholm, Sweden/Etats-Unis (3 aut., 11 aut., 12 aut.); Department of Biomathematics, UCLA School of Medicine/Los Angeles, California/Etats-Unis (5 aut., 6 aut.); Department of Radiological Sciences, UCLA School of Medicine/Los Angeles, California/Etats-Unis (10 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 5; Pp. 838-848; Bibl. 60 ref.
LA :	Anglais
EA :	Striatal 6-[¹⁸F]fluoro-L-DOPA (FDOPA) kinetic rate constants were measured by positron emission tomography (PET) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated squirrel monkeys. After scanning, stereological counts of dopaminergic neurons were done in substantia nigra, and dopamine (DA) and metabolite concentrations were determined in the caudate, putamen, and substantia nigra. Graded doses of MPTP produced animals with mild to moderate reductions (10-35%) in dopaminergic neurons, where the percent of cell loss was proportional to the amount of MPTP given. Striatal DA and metabolite concentrations were relatively unchanged in animals given 1.0 and 1.5 mg/kg of MPTP, but were significantly reduced after 2.0 mg/kg of MPTP. All animals injected with a single dose of MPTP showed no overt signs of parkinsonism. In contrast, DA and metabolite concentrations in the substantia nigra were significantly reduced for all MPTP-treated animals. Reduction of dopaminergic indices in the substantia nigra did not parallel reductions in the striatum, indicating differential sensitivity of the nigrostriatal pathway to the neurotoxic effects of MPTP. The percent change in FDOPA uptake (Ki) and decarboyxlation (k₃) after MPTP showed significant positive correlations to striatal DA levels, but not to the number of dopaminergic neurons. This suggests that FDOPA is a good index of striatal DA levels.
CC :	002B17G
FD :	Parkinson maladie; Stade clinique; Asymptomatique; Tomographie émission positon; Fluorodopa(18F); Locus niger; Stéréologie; Neurone dopaminergique; Modèle animal; Evolution; Cinétique; Singe; Animal
FG :	Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique
ED :	Parkinson disease; Clinical stage; Asymptomatic; Positron emission tomography; Fluorodopa(18F); Locus niger; Stereology; Dopaminergic neuron; Animal model; Evolution; Kinetics; Monkey; Animal
EG :	Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study
SD :	Parkinson enfermedad; Estadio clínico; Asintomático; Tomografía emisión positrones; Fluorodopa(18F); Locus níger; Estereología; Neurona dopaminérgica; Modelo animal; Evolución; Cinética; Mono; Animal
LO :	INIST-20953.354000099256460060
ID :	02-0049765

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Pascal:02-0049765

Le document en format XML

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<author><name sortKey="Langston, J W" sort="Langston, J W" uniqKey="Langston J" first="J. W." last="Langston">J. W. Langston</name>
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<author><name sortKey="Barrio, J R" sort="Barrio, J R" uniqKey="Barrio J" first="J. R." last="Barrio">J. R. Barrio</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Novel observations with FDOPA-PET imaging after early nigrostriatal damage</title>
<author><name sortKey="Yee, R E" sort="Yee, R E" uniqKey="Yee R" first="R. E." last="Yee">R. E. Yee</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Molecular and Medical Pharmacology, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
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<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, California</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
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<affiliation><inist:fA14 i1="03"><s1>Department of Neuroscience, Karolinska Institute</s1>
<s2>Stockholm, Sweden</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
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<affiliation><inist:fA14 i1="01"><s1>Department of Molecular and Medical Pharmacology, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
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<author><name sortKey="Huang, S C" sort="Huang, S C" uniqKey="Huang S" first="S-C." last="Huang">S-C. Huang</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Molecular and Medical Pharmacology, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
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<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>13 aut.</sZ>
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<affiliation><inist:fA14 i1="04"><s1>Department of Biomathematics, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<author><name sortKey="Shoghi Jadid, K" sort="Shoghi Jadid, K" uniqKey="Shoghi Jadid K" first="K." last="Shoghi-Jadid">K. Shoghi-Jadid</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Biomathematics, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<author><name sortKey="Satyamurthy, N" sort="Satyamurthy, N" uniqKey="Satyamurthy N" first="N." last="Satyamurthy">N. Satyamurthy</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Molecular and Medical Pharmacology, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>The Parkinson's Institute</s1>
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<affiliation><inist:fA14 i1="02"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, California</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
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<author><name sortKey="Farahani, K F" sort="Farahani, K F" uniqKey="Farahani K" first="K. F." last="Farahani">K. F. Farahani</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Radiological Sciences, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
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<author><name sortKey="Delfani, K" sort="Delfani, K" uniqKey="Delfani K" first="K." last="Delfani">K. Delfani</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroscience, Karolinska Institute</s1>
<s2>Stockholm, Sweden</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
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<author><name sortKey="Janson, A M" sort="Janson, A M" uniqKey="Janson A" first="A. M." last="Janson">A. M. Janson</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Neuroscience, Karolinska Institute</s1>
<s2>Stockholm, Sweden</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
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<affiliation><inist:fA14 i1="01"><s1>Department of Molecular and Medical Pharmacology, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, California</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
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<affiliation><inist:fA14 i1="01"><s1>Department of Molecular and Medical Pharmacology, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
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<series><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2001">2001</date>
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<term>Animal model</term>
<term>Asymptomatic</term>
<term>Clinical stage</term>
<term>Dopaminergic neuron</term>
<term>Evolution</term>
<term>Fluorodopa(18F)</term>
<term>Kinetics</term>
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<term>Neurone dopaminergique</term>
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<front><div type="abstract" xml:lang="en">Striatal 6-[<sup>18</sup>
F]fluoro-L-DOPA (FDOPA) kinetic rate constants were measured by positron emission tomography (PET) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated squirrel monkeys. After scanning, stereological counts of dopaminergic neurons were done in substantia nigra, and dopamine (DA) and metabolite concentrations were determined in the caudate, putamen, and substantia nigra. Graded doses of MPTP produced animals with mild to moderate reductions (10-35%) in dopaminergic neurons, where the percent of cell loss was proportional to the amount of MPTP given. Striatal DA and metabolite concentrations were relatively unchanged in animals given 1.0 and 1.5 mg/kg of MPTP, but were significantly reduced after 2.0 mg/kg of MPTP. All animals injected with a single dose of MPTP showed no overt signs of parkinsonism. In contrast, DA and metabolite concentrations in the substantia nigra were significantly reduced for all MPTP-treated animals. Reduction of dopaminergic indices in the substantia nigra did not parallel reductions in the striatum, indicating differential sensitivity of the nigrostriatal pathway to the neurotoxic effects of MPTP. The percent change in FDOPA uptake (Ki) and decarboyxlation (k<sub>3</sub>
) after MPTP showed significant positive correlations to striatal DA levels, but not to the number of dopaminergic neurons. This suggests that FDOPA is a good index of striatal DA levels.</div>
</front>
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<fA08 i1="01" i2="1" l="ENG"><s1>Novel observations with FDOPA-PET imaging after early nigrostriatal damage</s1>
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<fA14 i1="01"><s1>Department of Molecular and Medical Pharmacology, UCLA School of Medicine</s1>
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<fA14 i1="03"><s1>Department of Neuroscience, Karolinska Institute</s1>
<s2>Stockholm, Sweden</s2>
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<sZ>3 aut.</sZ>
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<sZ>12 aut.</sZ>
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<fA14 i1="04"><s1>Department of Biomathematics, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
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<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<fA14 i1="05"><s1>Department of Radiological Sciences, UCLA School of Medicine</s1>
<s2>Los Angeles, California</s2>
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<sZ>10 aut.</sZ>
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<fC01 i1="01" l="ENG"><s0>Striatal 6-[<sup>18</sup>
F]fluoro-L-DOPA (FDOPA) kinetic rate constants were measured by positron emission tomography (PET) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated squirrel monkeys. After scanning, stereological counts of dopaminergic neurons were done in substantia nigra, and dopamine (DA) and metabolite concentrations were determined in the caudate, putamen, and substantia nigra. Graded doses of MPTP produced animals with mild to moderate reductions (10-35%) in dopaminergic neurons, where the percent of cell loss was proportional to the amount of MPTP given. Striatal DA and metabolite concentrations were relatively unchanged in animals given 1.0 and 1.5 mg/kg of MPTP, but were significantly reduced after 2.0 mg/kg of MPTP. All animals injected with a single dose of MPTP showed no overt signs of parkinsonism. In contrast, DA and metabolite concentrations in the substantia nigra were significantly reduced for all MPTP-treated animals. Reduction of dopaminergic indices in the substantia nigra did not parallel reductions in the striatum, indicating differential sensitivity of the nigrostriatal pathway to the neurotoxic effects of MPTP. The percent change in FDOPA uptake (Ki) and decarboyxlation (k<sub>3</sub>
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<fC03 i1="05" i2="X" l="ENG"><s0>Fluorodopa(18F)</s0>
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<fC03 i1="05" i2="X" l="SPA"><s0>Fluorodopa(18F)</s0>
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<server><NO>PASCAL 02-0049765 INIST</NO>
<ET>Novel observations with FDOPA-PET imaging after early nigrostriatal damage</ET>
<AU>YEE (R. E.); IRWIN (I.); MILONAS (C.); STOUT (D. B.); HUANG (S-C.); SHOGHI-JADID (K.); SATYAMURTHY (N.); DELANNEY (L. E.); TOGASAKI (D. M.); FARAHANI (K. F.); DELFANI (K.); JANSON (A. M.); PHELPS (M. E.); LANGSTON (J. W.); BARRIO (J. R.)</AU>
<AF>Department of Molecular and Medical Pharmacology, UCLA School of Medicine/Los Angeles, California/Etats-Unis (1 aut., 4 aut., 5 aut., 7 aut., 13 aut., 15 aut.); The Parkinson's Institute/Sunnyvale, California/Etats-Unis (2 aut., 8 aut., 9 aut., 14 aut.); Department of Neuroscience, Karolinska Institute/Stockholm, Sweden/Etats-Unis (3 aut., 11 aut., 12 aut.); Department of Biomathematics, UCLA School of Medicine/Los Angeles, California/Etats-Unis (5 aut., 6 aut.); Department of Radiological Sciences, UCLA School of Medicine/Los Angeles, California/Etats-Unis (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 5; Pp. 838-848; Bibl. 60 ref.</SO>
<LA>Anglais</LA>
<EA>Striatal 6-[<sup>18</sup>
F]fluoro-L-DOPA (FDOPA) kinetic rate constants were measured by positron emission tomography (PET) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated squirrel monkeys. After scanning, stereological counts of dopaminergic neurons were done in substantia nigra, and dopamine (DA) and metabolite concentrations were determined in the caudate, putamen, and substantia nigra. Graded doses of MPTP produced animals with mild to moderate reductions (10-35%) in dopaminergic neurons, where the percent of cell loss was proportional to the amount of MPTP given. Striatal DA and metabolite concentrations were relatively unchanged in animals given 1.0 and 1.5 mg/kg of MPTP, but were significantly reduced after 2.0 mg/kg of MPTP. All animals injected with a single dose of MPTP showed no overt signs of parkinsonism. In contrast, DA and metabolite concentrations in the substantia nigra were significantly reduced for all MPTP-treated animals. Reduction of dopaminergic indices in the substantia nigra did not parallel reductions in the striatum, indicating differential sensitivity of the nigrostriatal pathway to the neurotoxic effects of MPTP. The percent change in FDOPA uptake (Ki) and decarboyxlation (k<sub>3</sub>
) after MPTP showed significant positive correlations to striatal DA levels, but not to the number of dopaminergic neurons. This suggests that FDOPA is a good index of striatal DA levels.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Stade clinique; Asymptomatique; Tomographie émission positon; Fluorodopa(18F); Locus niger; Stéréologie; Neurone dopaminergique; Modèle animal; Evolution; Cinétique; Singe; Animal</FD>
<FG>Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique</FG>
<ED>Parkinson disease; Clinical stage; Asymptomatic; Positron emission tomography; Fluorodopa(18F); Locus niger; Stereology; Dopaminergic neuron; Animal model; Evolution; Kinetics; Monkey; Animal</ED>
<EG>Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study</EG>
<SD>Parkinson enfermedad; Estadio clínico; Asintomático; Tomografía emisión positrones; Fluorodopa(18F); Locus níger; Estereología; Neurona dopaminérgica; Modelo animal; Evolución; Cinética; Mono; Animal</SD>
<LO>INIST-20953.354000099256460060</LO>
<ID>02-0049765</ID>
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Movement Disorders (revue)

Novel observations with FDOPA-PET imaging after early nigrostriatal damage

Novel observations with FDOPA-PET imaging after early nigrostriatal damage

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