Uneven age effects of [18F]FP-CIT binding in the striatum of Parkinson’s disease
Objective Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We investigated if similar changes occur in the striatum of Parkinson’s disease (PD) patients, using PET and [ 18 F]FP-CIT, a ligand for DAT. M...
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Published in | Annals of nuclear medicine Vol. 28; no. 9; pp. 874 - 879 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Tokyo
Springer Japan
01.11.2014
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
ISSN | 0914-7187 1864-6433 |
DOI | 10.1007/s12149-014-0882-1 |
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Abstract | Objective
Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We investigated if similar changes occur in the striatum of Parkinson’s disease (PD) patients, using PET and [
18
F]FP-CIT, a ligand for DAT.
Methods
We performed [
18
F]FP-CIT PET in 39 drug-naïve, de novo PD patients (age 56.0 ± 11.6 years, mean ± SD) and 34 healthy control subjects (age 52.3 ± 17.8). Parkinsonism was assessed by UPDRS III and Purdue pegboard. Binding ratios of [
18
F]FP-CIT were obtained in the putamen and caudate using the occipital cortex as reference.
Results
Mean [
18
F]FP-CIT binding ratios in PD were 3.76 ± 0.74 (mean ± SD) in the putamen and 6.80 ± 1.05 in the caudate nucleus, significantly smaller than those in the healthy control (9.20 ± 1.38, 8.66 ± 1.12, respectively;
p
< 0.001 vs. healthy control for both). Regression analysis of [
18
F]FP-CIT binding ratios on age in healthy subjects showed significant correlations in the putamen (
p
< 0.001) and caudate nucleus (
p
< 0.001). Similar analysis in PD patients also showed significant correlations in the putamen (
p
= 0.015) and caudate nucleus (
p
= 0.018). The slope of regression in the putamen was −0.061 in the healthy control and −0.017 in PD, with significant differences between the two groups (
p
= 0.0003). In contrast, the regression slope in the caudate nucleus was −0.040 in the healthy control group, and −0.032 in the PD group with no significant differences between the two groups.
Conclusions
Striatal [
18
F]FP-CIT binding showed significant age affects in patients with de novo PD after standardization for the severity of disease. The age effects were significantly smaller in PD patients than those in healthy subjects, but only in the putamen, not in the caudate nucleus. Given that age-related attrition of DA neurons is even in normal striatum, the uneven age effects in the parkinsonian striatum are likely to reflect the superimposition of disease-driven compensation on the aging effect. |
---|---|
AbstractList | Objective
Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We investigated if similar changes occur in the striatum of Parkinson’s disease (PD) patients, using PET and [
18
F]FP-CIT, a ligand for DAT.
Methods
We performed [
18
F]FP-CIT PET in 39 drug-naïve, de novo PD patients (age 56.0 ± 11.6 years, mean ± SD) and 34 healthy control subjects (age 52.3 ± 17.8). Parkinsonism was assessed by UPDRS III and Purdue pegboard. Binding ratios of [
18
F]FP-CIT were obtained in the putamen and caudate using the occipital cortex as reference.
Results
Mean [
18
F]FP-CIT binding ratios in PD were 3.76 ± 0.74 (mean ± SD) in the putamen and 6.80 ± 1.05 in the caudate nucleus, significantly smaller than those in the healthy control (9.20 ± 1.38, 8.66 ± 1.12, respectively;
p
< 0.001 vs. healthy control for both). Regression analysis of [
18
F]FP-CIT binding ratios on age in healthy subjects showed significant correlations in the putamen (
p
< 0.001) and caudate nucleus (
p
< 0.001). Similar analysis in PD patients also showed significant correlations in the putamen (
p
= 0.015) and caudate nucleus (
p
= 0.018). The slope of regression in the putamen was −0.061 in the healthy control and −0.017 in PD, with significant differences between the two groups (
p
= 0.0003). In contrast, the regression slope in the caudate nucleus was −0.040 in the healthy control group, and −0.032 in the PD group with no significant differences between the two groups.
Conclusions
Striatal [
18
F]FP-CIT binding showed significant age affects in patients with de novo PD after standardization for the severity of disease. The age effects were significantly smaller in PD patients than those in healthy subjects, but only in the putamen, not in the caudate nucleus. Given that age-related attrition of DA neurons is even in normal striatum, the uneven age effects in the parkinsonian striatum are likely to reflect the superimposition of disease-driven compensation on the aging effect. Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We investigated if similar changes occur in the striatum of Parkinson's disease (PD) patients, using PET and [(18)F]FP-CIT, a ligand for DAT. We performed [(18)F]FP-CIT PET in 39 drug-naïve, de novo PD patients (age 56.0 ± 11.6 years, mean ± SD) and 34 healthy control subjects (age 52.3 ± 17.8). Parkinsonism was assessed by UPDRS III and Purdue pegboard. Binding ratios of [(18)F]FP-CIT were obtained in the putamen and caudate using the occipital cortex as reference. Mean [(18)F]FP-CIT binding ratios in PD were 3.76 ± 0.74 (mean ± SD) in the putamen and 6.80 ± 1.05 in the caudate nucleus, significantly smaller than those in the healthy control (9.20 ± 1.38, 8.66 ± 1.12, respectively; p < 0.001 vs. healthy control for both). Regression analysis of [(18)F]FP-CIT binding ratios on age in healthy subjects showed significant correlations in the putamen (p < 0.001) and caudate nucleus (p < 0.001). Similar analysis in PD patients also showed significant correlations in the putamen (p = 0.015) and caudate nucleus (p = 0.018). The slope of regression in the putamen was -0.061 in the healthy control and -0.017 in PD, with significant differences between the two groups (p = 0.0003). In contrast, the regression slope in the caudate nucleus was -0.040 in the healthy control group, and -0.032 in the PD group with no significant differences between the two groups. Striatal [(18)F]FP-CIT binding showed significant age affects in patients with de novo PD after standardization for the severity of disease. The age effects were significantly smaller in PD patients than those in healthy subjects, but only in the putamen, not in the caudate nucleus. Given that age-related attrition of DA neurons is even in normal striatum, the uneven age effects in the parkinsonian striatum are likely to reflect the superimposition of disease-driven compensation on the aging effect. Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We investigated if similar changes occur in the striatum of Parkinson's disease (PD) patients, using PET and [^sup 18^F]FP-CIT, a ligand for DAT. We performed [^sup 18^F]FP-CIT PET in 39 drug-naïve, de novo PD patients (age 56.0 ± 11.6 years, mean ± SD) and 34 healthy control subjects (age 52.3 ± 17.8). Parkinsonism was assessed by UPDRS III and Purdue pegboard. Binding ratios of [^sup 18^F]FP-CIT were obtained in the putamen and caudate using the occipital cortex as reference. Mean [^sup 18^F]FP-CIT binding ratios in PD were 3.76 ± 0.74 (mean ± SD) in the putamen and 6.80 ± 1.05 in the caudate nucleus, significantly smaller than those in the healthy control (9.20 ± 1.38, 8.66 ± 1.12, respectively; p < 0.001 vs. healthy control for both). Regression analysis of [^sup 18^F]FP-CIT binding ratios on age in healthy subjects showed significant correlations in the putamen (p < 0.001) and caudate nucleus (p < 0.001). Similar analysis in PD patients also showed significant correlations in the putamen (p = 0.015) and caudate nucleus (p = 0.018). The slope of regression in the putamen was -0.061 in the healthy control and -0.017 in PD, with significant differences between the two groups (p = 0.0003). In contrast, the regression slope in the caudate nucleus was -0.040 in the healthy control group, and -0.032 in the PD group with no significant differences between the two groups. Striatal [^sup 18^F]FP-CIT binding showed significant age affects in patients with de novo PD after standardization for the severity of disease. The age effects were significantly smaller in PD patients than those in healthy subjects, but only in the putamen, not in the caudate nucleus. Given that age-related attrition of DA neurons is even in normal striatum, the uneven age effects in the parkinsonian striatum are likely to reflect the superimposition of disease-driven compensation on the aging effect.[PUBLICATION ABSTRACT] Objective: Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We investigated if similar changes occur in the striatum of Parkinson's disease (PD) patients, using PET and [ super(18)F]FP-CIT, a ligand for DAT. Methods: We performed [ super(18)F]FP-CIT PET in 39 drug-naive, de novo PD patients (age 56.0 plus or minus 11.6 years, mean plus or minus SD) and 34 healthy control subjects (age 52.3 plus or minus 17.8). Parkinsonism was assessed by UPDRS III and Purdue pegboard. Binding ratios of [ super(18)F]FP-CIT were obtained in the putamen and caudate using the occipital cortex as reference. Results: Mean [ super(18)F]FP-CIT binding ratios in PD were 3.76 plus or minus 0.74 (mean plus or minus SD) in the putamen and 6.80 plus or minus 1.05 in the caudate nucleus, significantly smaller than those in the healthy control (9.20 plus or minus 1.38, 8.66 plus or minus 1.12, respectively; p < 0.001 vs. healthy control for both). Regression analysis of [ super(18)F]FP-CIT binding ratios on age in healthy subjects showed significant correlations in the putamen (p < 0.001) and caudate nucleus (p < 0.001). Similar analysis in PD patients also showed significant correlations in the putamen (p = 0.015) and caudate nucleus (p = 0.018). The slope of regression in the putamen was -0.061 in the healthy control and -0.017 in PD, with significant differences between the two groups (p = 0.0003). In contrast, the regression slope in the caudate nucleus was -0.040 in the healthy control group, and -0.032 in the PD group with no significant differences between the two groups. Conclusions: Striatal [ super(18)F]FP-CIT binding showed significant age affects in patients with de novo PD after standardization for the severity of disease. The age effects were significantly smaller in PD patients than those in healthy subjects, but only in the putamen, not in the caudate nucleus. Given that age-related attrition of DA neurons is even in normal striatum, the uneven age effects in the parkinsonian striatum are likely to reflect the superimposition of disease-driven compensation on the aging effect. |
Author | Kim, Su-Jeong Yun, Sung-Cheol Kim, Jae Seung Oh, Seung Jun Doudet, Doris Kim, Hye Ok Lee, Chong S. |
Author_xml | – sequence: 1 givenname: Chong S. surname: Lee fullname: Lee, Chong S. organization: Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine – sequence: 2 givenname: Su-Jeong surname: Kim fullname: Kim, Su-Jeong organization: Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine – sequence: 3 givenname: Seung Jun surname: Oh fullname: Oh, Seung Jun organization: Department of Nuclear Medicine, Asan Medical Center, University of Ulsan College of Medicine – sequence: 4 givenname: Hye Ok surname: Kim fullname: Kim, Hye Ok organization: Department of Nuclear Medicine, Asan Medical Center, University of Ulsan College of Medicine – sequence: 5 givenname: Sung-Cheol surname: Yun fullname: Yun, Sung-Cheol organization: Department of Clinical Epidemiology and Biostatistics, Asan Medical Center, University of Ulsan College of Medicine – sequence: 6 givenname: Doris surname: Doudet fullname: Doudet, Doris organization: Department of Medicine/Neurology, University of British Columbia – sequence: 7 givenname: Jae Seung surname: Kim fullname: Kim, Jae Seung email: jaeskim@amc.seoul.kr organization: Department of Nuclear Medicine, Asan Medical Center, University of Ulsan College of Medicine |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25008292$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1007_s12149_022_01818_5 crossref_primary_10_1186_s13550_024_01126_1 crossref_primary_10_1007_s13139_017_0481_x crossref_primary_10_1097_MNM_0000000000001098 crossref_primary_10_1007_s00415_020_09788_2 crossref_primary_10_1007_s13139_024_00840_x crossref_primary_10_1038_s41598_019_47026_6 crossref_primary_10_3390_ijms222011234 crossref_primary_10_14802_jmd_15031 crossref_primary_10_3390_cells8080872 crossref_primary_10_1016_j_neurobiolaging_2015_01_016 |
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Keywords | Dopamine transporter [ Positron emission tomography Age Parkinson’s disease F]FP-CIT |
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Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We... Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes. We... Objective: Dopamine transporter (DAT) imaging shows age-related decline of ligand binding in the normal striatum, a decline attributed to regulatory changes.... |
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SubjectTerms | Adult Aged Aging - physiology Corpus Striatum - diagnostic imaging Corpus Striatum - physiopathology Female Humans Imaging Male Medicine Medicine & Public Health Middle Aged Nuclear Medicine Original Article Parkinson Disease - diagnostic imaging Parkinson Disease - physiopathology Positron-Emission Tomography Radiology Radiopharmaceuticals - pharmacokinetics Regression Analysis Severity of Illness Index Tropanes - pharmacokinetics |
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Title | Uneven age effects of [18F]FP-CIT binding in the striatum of Parkinson’s disease |
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