A within-subject comparison of 6-[18F]fluoro-m-tyrosine and 6-[18F]fluoro-L-dopa in Parkinson's disease
Progression of Parkinson's disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The radiopharmaceutical 6‐[18F]fluoro‐m‐tyrosine is not a substrate for catechol‐O‐methyltransferase and therefore has a more favorable uptake‐t...
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| Published in | Movement disorders Vol. 26; no. 11; pp. 2032 - 2038 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.09.2011
Wiley |
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| Online Access | Get full text |
| ISSN | 0885-3185 1531-8257 |
| DOI | 10.1002/mds.23778 |
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| Abstract | Progression of Parkinson's disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The radiopharmaceutical 6‐[18F]fluoro‐m‐tyrosine is not a substrate for catechol‐O‐methyltransferase and therefore has a more favorable uptake‐to‐background ratio than 6‐[18F]fluoro‐L‐dopa. The objective of this study was to evaluate 6‐[18F]fluoro‐m‐tyrosine relative to 6‐[18F]fluoro‐L‐dopa with partial catechol‐O‐methyltransferase inhibition as a biomarker for clinical status in Parkinson's disease. Twelve patients with early‐stage Parkinson's disease, off medication, underwent Unified Parkinson Disease Rating Scale scoring, brain magnetic resonance imaging, and 3‐dimensional dynamic positron emission tomography using equivalent doses of 6‐[18F]fluoro‐m‐tyrosine and 6‐[18F]fluoro‐L‐dopa with tolcapone, a catechol‐O‐methyltransferase inhibitor. Images were realigned within subject, after which the tissue‐derived uptake rate constant was generated for volumes of interest encompassing the caudate nucleus, putamen, and subregions of the putamen. We computed both bivariate (Pearson) and partial (covariate of age) correlations between clinical subscores and tissue‐derived uptake rate constant. Tissue‐derived uptake rate constant values were correlated between the radiopharmaceuticals (r = 0.8). Motor subscores were inversely correlated with the contralateral putamen 6‐[18F]fluoro‐m‐tyrosine tissue‐derived uptake rate constant (|r| > 0.72, P < .005) but not significantly with the 6‐[18F]fluoro‐L‐dopa tissue‐derived uptake rate constant. The uptake rate constants for both radiopharmaceuticals were also inversely correlated with activities of daily living subscores, but the magnitude of correlation coefficients was greater for 6‐[18F]fluoro‐m‐tyrosine. In this design, 6‐[18F]fluoro‐m‐tyrosine uptake better reflected clinical status than did 6‐[18F]fluoro‐L‐dopa uptake. We attribute this finding to 6‐[18F]fluoro‐m‐tyrosine's higher affinity for the target, L‐aromatic amino acid decarboxylase, and the absence of other major determinants of the uptake rate constant. These results also imply that L‐aromatic amino acid decarboxylase activity is a major determinant of clinical status. © 2011 Movement Disorder Society |
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| AbstractList | Progression of Parkinson's disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The radiopharmaceutical 6‐[18F]fluoro‐m‐tyrosine is not a substrate for catechol‐O‐methyltransferase and therefore has a more favorable uptake‐to‐background ratio than 6‐[18F]fluoro‐L‐dopa. The objective of this study was to evaluate 6‐[18F]fluoro‐m‐tyrosine relative to 6‐[18F]fluoro‐L‐dopa with partial catechol‐O‐methyltransferase inhibition as a biomarker for clinical status in Parkinson's disease. Twelve patients with early‐stage Parkinson's disease, off medication, underwent Unified Parkinson Disease Rating Scale scoring, brain magnetic resonance imaging, and 3‐dimensional dynamic positron emission tomography using equivalent doses of 6‐[18F]fluoro‐m‐tyrosine and 6‐[18F]fluoro‐L‐dopa with tolcapone, a catechol‐O‐methyltransferase inhibitor. Images were realigned within subject, after which the tissue‐derived uptake rate constant was generated for volumes of interest encompassing the caudate nucleus, putamen, and subregions of the putamen. We computed both bivariate (Pearson) and partial (covariate of age) correlations between clinical subscores and tissue‐derived uptake rate constant. Tissue‐derived uptake rate constant values were correlated between the radiopharmaceuticals (r = 0.8). Motor subscores were inversely correlated with the contralateral putamen 6‐[18F]fluoro‐m‐tyrosine tissue‐derived uptake rate constant (|r| > 0.72, P < .005) but not significantly with the 6‐[18F]fluoro‐L‐dopa tissue‐derived uptake rate constant. The uptake rate constants for both radiopharmaceuticals were also inversely correlated with activities of daily living subscores, but the magnitude of correlation coefficients was greater for 6‐[18F]fluoro‐m‐tyrosine. In this design, 6‐[18F]fluoro‐m‐tyrosine uptake better reflected clinical status than did 6‐[18F]fluoro‐L‐dopa uptake. We attribute this finding to 6‐[18F]fluoro‐m‐tyrosine's higher affinity for the target, L‐aromatic amino acid decarboxylase, and the absence of other major determinants of the uptake rate constant. These results also imply that L‐aromatic amino acid decarboxylase activity is a major determinant of clinical status. © 2011 Movement Disorder Society Progression of Parkinson’s disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The radiopharmaceutical 6-[ 18 F]fluoro-m-tyrosine is not a substrate for catechol-O-methyltransferase and therefore has a more favorable uptake-to-background ratio than 6-[ 18 F]fluoro- l -dopa. The objective of this study was to evaluate 6-[ 18 F]fluoro-m-tyrosine relative to 6-[ 18 F]fluoro- l -dopa with partial catechol- O -methyltransferase inhibition as a biomarker for clinical status in Parkinson’s disease. Twelve patients with early-stage Parkinson’s disease, off medication, underwent Unified Parkinson Disease Rating Scale scoring, brain magnetic resonance imaging, and 3-dimensional dynamic positron emission tomography using equivalent doses of 6-[ 18 F]fluoro-m-tyrosine and 6-[ 18 F]fluoro- l -dopa with tolcapone, a catechol- O -methyltransferase inhibitor. Images were realigned within subject, after which the tissue-derived uptake rate constant was generated for volumes of interest encompassing the caudate nucleus, putamen, and subregions of the putamen. We computed both bivariate (Pearson) and partial (covariate of age) correlations between clinical subscores and tissue-derived uptake rate constant. Tissue-derived uptake rate constant values were correlated between the radiopharmaceuticals ( r = 0.8). Motor subscores were inversely correlated with the contralateral putamen 6-[ 18 F]fluoro-m-tyrosine tissue-derived uptake rate constant (|r| > 0.72, P < .005) but not significantly with the 6-[ 18 F]fluoro- l -dopa tissue- derived uptake rate constant. The uptake rate constants for both radiopharmaceuticals were also inversely correlated with activities of daily living subscores, but the magnitude of correlation coefficients was greater for 6-[ 18 F]fluoro-m-tyrosine. In this design, 6-[ 18 F]fluoro-m-tyrosine uptake better reflected clinical status than did 6-[ 18 F]fluoro- l -dopa uptake. We attribute this finding to 6-[ 18 F]fluoro-m-tyrosine’s higher affinity for the target, l -aromatic amino acid decarboxylase, and the absence of other major determinants of the uptake rate constant. These results also imply that l -aromatic amino acid decarboxylase activity is a major determinant of clinical status. Progression of Parkinson's disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The radiopharmaceutical 6‐[ 18 F]fluoro‐m‐tyrosine is not a substrate for catechol‐ O ‐methyltransferase and therefore has a more favorable uptake‐to‐background ratio than 6‐[ 18 F]fluoro‐ L ‐dopa. The objective of this study was to evaluate 6‐[ 18 F]fluoro‐m‐tyrosine relative to 6‐[ 18 F]fluoro‐ L ‐dopa with partial catechol‐ O ‐methyltransferase inhibition as a biomarker for clinical status in Parkinson's disease. Twelve patients with early‐stage Parkinson's disease, off medication, underwent Unified Parkinson Disease Rating Scale scoring, brain magnetic resonance imaging, and 3‐dimensional dynamic positron emission tomography using equivalent doses of 6‐[ 18 F]fluoro‐m‐tyrosine and 6‐[ 18 F]fluoro‐ L ‐dopa with tolcapone, a catechol‐ O ‐methyltransferase inhibitor. Images were realigned within subject, after which the tissue‐derived uptake rate constant was generated for volumes of interest encompassing the caudate nucleus, putamen, and subregions of the putamen. We computed both bivariate (Pearson) and partial (covariate of age) correlations between clinical subscores and tissue‐derived uptake rate constant. Tissue‐derived uptake rate constant values were correlated between the radiopharmaceuticals ( r = 0.8). Motor subscores were inversely correlated with the contralateral putamen 6‐[ 18 F]fluoro‐m‐tyrosine tissue‐derived uptake rate constant (|r| > 0.72, P < .005) but not significantly with the 6‐[ 18 F]fluoro‐ L ‐dopa tissue‐derived uptake rate constant. The uptake rate constants for both radiopharmaceuticals were also inversely correlated with activities of daily living subscores, but the magnitude of correlation coefficients was greater for 6‐[ 18 F]fluoro‐m‐tyrosine. In this design, 6‐[ 18 F]fluoro‐m‐tyrosine uptake better reflected clinical status than did 6‐[ 18 F]fluoro‐ L ‐dopa uptake. We attribute this finding to 6‐[ 18 F]fluoro‐m‐tyrosine's higher affinity for the target, L ‐aromatic amino acid decarboxylase, and the absence of other major determinants of the uptake rate constant. These results also imply that L ‐aromatic amino acid decarboxylase activity is a major determinant of clinical status. © 2011 Movement Disorder Society Progression of Parkinson's disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The radiopharmaceutical 6-[(18) F]fluoro-m-tyrosine is not a substrate for catechol-O-methyltransferase and therefore has a more favorable uptake-to-background ratio than 6-[(18) F]fluoro-L-dopa. The objective of this study was to evaluate 6-[(18) F]fluoro-m-tyrosine relative to 6-[(18) F]fluoro-L-dopa with partial catechol-O-methyltransferase inhibition as a biomarker for clinical status in Parkinson's disease. Twelve patients with early-stage Parkinson's disease, off medication, underwent Unified Parkinson Disease Rating Scale scoring, brain magnetic resonance imaging, and 3-dimensional dynamic positron emission tomography using equivalent doses of 6-[(18) F]fluoro-m-tyrosine and 6-[(18) F]fluoro-L-dopa with tolcapone, a catechol-O-methyltransferase inhibitor. Images were realigned within subject, after which the tissue-derived uptake rate constant was generated for volumes of interest encompassing the caudate nucleus, putamen, and subregions of the putamen. We computed both bivariate (Pearson) and partial (covariate of age) correlations between clinical subscores and tissue-derived uptake rate constant. Tissue-derived uptake rate constant values were correlated between the radiopharmaceuticals (r = 0.8). Motor subscores were inversely correlated with the contralateral putamen 6-[(18) F]fluoro-m-tyrosine tissue-derived uptake rate constant (|r| > 0.72, P < .005) but not significantly with the 6-[(18) F]fluoro-L-dopa tissue-derived uptake rate constant. The uptake rate constants for both radiopharmaceuticals were also inversely correlated with activities of daily living subscores, but the magnitude of correlation coefficients was greater for 6-[(18) F]fluoro-m-tyrosine. In this design, 6-[(18) F]fluoro-m-tyrosine uptake better reflected clinical status than did 6-[(18) F]fluoro-L-dopa uptake. We attribute this finding to 6-[(18) F]fluoro-m-tyrosine's higher affinity for the target, L-aromatic amino acid decarboxylase, and the absence of other major determinants of the uptake rate constant. These results also imply that L-aromatic amino acid decarboxylase activity is a major determinant of clinical status. |
| Author | Bendlin, Barbara B. Stone, Charles K. Buyan-Dent, Laura Johnson, Sterling C. Dejesus, Onofre T. Harding, Sandra J. Holden, James E. Nickles, Robert J. Christian, Bradley T. Gallagher, Catherine L. Mueller, Barb |
| AuthorAffiliation | 2 Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA 5 William S. Middleton Veterans Hospital G.R.E.C.C., Madison, Wisconsin, USA 1 William S. Middleton Veterans Hospital, Madison, Wisconsin, USA 3 University of Wisconsin, Department of Medical Physics, Madison, Wisconsin, USA 4 Waisman Laboratory for Brain Imaging and Behavior, Madison, Wisconsin, USA 6 Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA |
| AuthorAffiliation_xml | – name: 1 William S. Middleton Veterans Hospital, Madison, Wisconsin, USA – name: 3 University of Wisconsin, Department of Medical Physics, Madison, Wisconsin, USA – name: 5 William S. Middleton Veterans Hospital G.R.E.C.C., Madison, Wisconsin, USA – name: 2 Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA – name: 4 Waisman Laboratory for Brain Imaging and Behavior, Madison, Wisconsin, USA – name: 6 Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA |
| Author_xml | – sequence: 1 givenname: Catherine L. surname: Gallagher fullname: Gallagher, Catherine L. email: gallagher@neurology.wisc.edu organization: William S. Middleton Veterans Hospital, Madison, Wisconsin, USA – sequence: 2 givenname: Bradley T. surname: Christian fullname: Christian, Bradley T. organization: University of Wisconsin, Department of Medical Physics, Madison, Wisconsin, USA – sequence: 3 givenname: James E. surname: Holden fullname: Holden, James E. organization: University of Wisconsin, Department of Medical Physics, Madison, Wisconsin, USA – sequence: 4 givenname: Onofre T. surname: Dejesus fullname: Dejesus, Onofre T. organization: University of Wisconsin, Department of Medical Physics, Madison, Wisconsin, USA – sequence: 5 givenname: Robert J. surname: Nickles fullname: Nickles, Robert J. organization: University of Wisconsin, Department of Medical Physics, Madison, Wisconsin, USA – sequence: 6 givenname: Laura surname: Buyan-Dent fullname: Buyan-Dent, Laura organization: Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA – sequence: 7 givenname: Barbara B. surname: Bendlin fullname: Bendlin, Barbara B. organization: William S. Middleton Veterans Hospital G.R.E.C.C., Madison, Wisconsin, USA – sequence: 8 givenname: Sandra J. surname: Harding fullname: Harding, Sandra J. organization: William S. Middleton Veterans Hospital G.R.E.C.C., Madison, Wisconsin, USA – sequence: 9 givenname: Charles K. surname: Stone fullname: Stone, Charles K. organization: Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA – sequence: 10 givenname: Barb surname: Mueller fullname: Mueller, Barb organization: Waisman Laboratory for Brain Imaging and Behavior, Madison, Wisconsin, USA – sequence: 11 givenname: Sterling C. surname: Johnson fullname: Johnson, Sterling C. organization: William S. Middleton Veterans Hospital G.R.E.C.C., Madison, Wisconsin, USA |
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| Copyright | Copyright © 2011 Movement Disorder Society 2015 INIST-CNRS Copyright © 2011 Movement Disorder Society. 2011 Disorder Society 2011 |
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| Keywords | Human Tyrosine Nervous system diseases Dopamine Parkinson disease Catecholamine Fluorodopa (18F) Metabolism Parkinson's disease/radionuclide imaging Cerebral disorder dopamine/metabolism Central nervous system disease Neurotransmitter Degenerative disease Levodopa Positron emission tomography Comparative study Extrapyramidal syndrome Emission tomography |
| Language | English |
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| Notes | Funding agencies: This work was supported by the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Clinical Science Research and Development Service and University of Wisconsin Institute for Clinical and Translational Research, funded through a National Institutes of Health Clinical and Translational Science Award (grant number 1UL1RR025011). This work was supported with the use of facilities at the William S. Middleton Memorial Veterans Hospital Geriatric Research Education and Clinical Center and the Waisman Laboratory for Brain Imaging and Behavior, Madison, Wisconsin. Full financial disclosures and author roles may be found in the online version of this article. ark:/67375/WNG-688RJFBJ-N Relevant conflicts of interest/financial disclosures: Nothing to report. ArticleID:MDS23778 istex:522EE64365D119496B962B5766EE5C0A818FA428 Nothing to report. This work was supported by the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Clinical Science Research and Development Service and University of Wisconsin Institute for Clinical and Translational Research, funded through a National Institutes of Health Clinical and Translational Science Award (grant number 1UL1RR025011). This work was supported with the use of facilities at the William S. Middleton Memorial Veterans Hospital Geriatric Research Education and Clinical Center and the Waisman Laboratory for Brain Imaging and Behavior, Madison, Wisconsin. Relevant conflicts of interest/financial disclosures Funding agencies |
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Exp Neurol 2000; 165: 342-346. 1987; 14 1997; 60 1985; 5 2010 1995; 37 1997; 41 1993; 44 2006; 14 2005; 62 1994; 44 2003; 59 1995 2003; 18 1988; 51 1999; 40 2002 2008; 70 2003; 54 2001; 21 2004; 52 1998; 39 2005; 19 1979; 45 2009; 73 1988; 29 1999; 19 2006; 21 1990; 28 1992; 597 1984; 35 2002; 22 2008; 28 1987 2001; 16 2000; 165 1998; 51 1992; 89 1996; 119 e_1_2_6_31_2 e_1_2_6_30_2 Asselin R (e_1_2_6_9_2) 2002 e_1_2_6_18_2 e_1_2_6_19_2 Thomas SR (e_1_2_6_21_2) 1999; 40 Firnau G (e_1_2_6_27_2) 1988; 29 e_1_2_6_12_2 e_1_2_6_35_2 e_1_2_6_13_2 e_1_2_6_34_2 e_1_2_6_10_2 e_1_2_6_33_2 e_1_2_6_11_2 e_1_2_6_32_2 e_1_2_6_16_2 Brown WD (e_1_2_6_22_2) 1998; 39 e_1_2_6_39_2 e_1_2_6_17_2 e_1_2_6_38_2 e_1_2_6_14_2 e_1_2_6_37_2 e_1_2_6_15_2 e_1_2_6_36_2 Garnett ES (e_1_2_6_24_2) 1987; 14 Dejesus OT (e_1_2_6_29_2) 1995; 37 e_1_2_6_20_2 e_1_2_6_40_2 e_1_2_6_8_2 e_1_2_6_7_2 e_1_2_6_4_2 e_1_2_6_3_2 e_1_2_6_6_2 e_1_2_6_5_2 e_1_2_6_23_2 e_1_2_6_2_2 e_1_2_6_28_2 e_1_2_6_26_2 e_1_2_6_25_2 |
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| Snippet | Progression of Parkinson's disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The... Progression of Parkinson’s disease symptoms is imperfectly correlated with positron emission tomography biomarkers for dopamine biosynthetic pathways. The... |
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| SubjectTerms | Aged Biological and medical sciences Brain - diagnostic imaging Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dihydroxyphenylalanine - analogs & derivatives Dihydroxyphenylalanine - pharmacokinetics dopamine/metabolism Female Fluorine Radioisotopes Humans Male Medical sciences Middle Aged Neurology Parkinson Disease - diagnostic imaging Parkinson Disease - pathology Parkinson's disease/radionuclide imaging positron emission tomography Severity of Illness Index Tomography, Emission-Computed Tyrosine - analogs & derivatives Tyrosine - pharmacokinetics |
| Title | A within-subject comparison of 6-[18F]fluoro-m-tyrosine and 6-[18F]fluoro-L-dopa in Parkinson's disease |
| URI | https://api.istex.fr/ark:/67375/WNG-688RJFBJ-N/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fmds.23778 https://www.ncbi.nlm.nih.gov/pubmed/21638324 https://pubmed.ncbi.nlm.nih.gov/PMC3278160 |
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