Abstract
Loss of striatal dopamine (DA) transporters in Parkinson's disease (PD) has been accurately assessed in vivo by single-photon emission tomography (SPET) studies using [123I]β-CIT. However, these studies have also shown that adequate imaging of the striatal DA transporter content can be performed only 20–30 h following the injection of [123I]β-CIT, which is not convenient for routine out-patient evaluations. Recently, a new ligand,N-ω-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)tropane (FP-CIT), became available for in vivo imaging of the DA transporter. The faster kinetics of [123I]FP-CIT have been shown to allow adequate acquisition as early as 3 h following injection. In the present study, loss of striatal DA transporters in five non-medicated PD patients was assessed on two consecutive SPET scans, one with [123I]β-CIT (24 h following injection) and one with [123I]FP-CIT (3 h following injection). The ratios of specific to non-specific [123I]FP-CIT uptake in the caudate nucleus and putamen were consistently 2.5-fold lower than those of [123I]β-CIT. However, when the uptake ratio of both ligands in these brain regions of patients was expressed as a percentage of the uptake ratio found in healthy controls, both the decrease and the variation of the data were similar. It is concluded on the basis of these findings that [123I]FP-CIT seems as good as [123I]β-CIT for the assessment of the dopaminergic deficit in PD. The faster kinetics of [123I]FP-CIT are a clear advantage.
References
Brücke T, Kornhuber J, Angelberger P, Asenbaum S, Frassine H, Podreka I. SPECT imaging of dopamine and serotonin transporters with [123I]β-CIT. Binding kinetics in the human brain.J Neural Transm [Gen Sect] 1993; 94: 137–146.
Seibyl JP, Marek KL, Quinlan D, et al. Decreased single-photon emission computed tomographic [123I]β-CIT striatal uptake correlates with symptom severity in Parkinson's disease.Ann Neurol 1995; 38: 589–598.
Vermeulen RJ, Wolters EC, Tissingh E, et al. Evaluation of [123I]β-CIT binding with SPECT in controls, early and late Parkinson's disease.Nucl Med Biol 1995; 22: 985–991.
Laruelle M, Wallace E, Seibyl JP, et al. Graphical, kinetic and equilibrium analysis of [123I]β-CIT in vivo binding to dopamine transporters in healthy subjects.J Cereb Blood Flow Metab 1994; 14: 982–994.
Baldwin RM, Zea-Ponce Y, Al-Tikriti MS, et al. Regional brain uptake and pharmacokinetics of [123I]N-ω-fluoroalkyl-2β-carboxy-3β-(4-iodophenyl)nortropane esters in baboons.Nucl Med Biol 1995; 22: 211–219.
Neumeyer JL, Wang S, Gao Y, et al.N-ω-fluoroalkyl analogs of (1R)-2β-carbomethoxy-3-β-(4-iodophenyl)-tropane (β-CIT): radiotracers for positron emission tomography and single photon emission computed tomography imaging of dopamine transporters.J Med Chem 1994; 37: 1558–1561.
Lundkvist C, Halldin C, Swahn C-G, et al. [O-methyl-11C]β-CIT-FP, a potential radioligand for quantitation of the dopamine transporter: preparation, autoradiography, metabolic studies, and positron emission tomography examinations.Nucl Med Biol 1995; 22: 905–913.
Abi-Dargham A, Gandelman MS, DeErausquin GA, et al. SPECT imaging of dopamine transporters in human brain with iodine-123-fluoroalkyl analogs of β-CIT.J Nucl Med 1996; 37: 1129–1133.
Kuikka JT, Bergström KA, Ahonen A, et al. Comparison of iodine-123 labelled 2β-carbomethocy-3β-(4-iodophenyl)tropane and 2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl)nortropane for imaging of the dopamine transporter in the living human brain.Eur J Nucl Med 1995; 22: 356–360.
Booij J, Tissingh G, Boer GJ, et al. [123I]FP-CIT SPECT reveals marked decline of striatal dopamine transporter labelling in early and advanced Parkinson's disease. J Neurol Neurosurg Psychiatry 1996; in press.
Gibb WRG, Lees AJ. The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson's disease.J Neurol Neurosurg Psychiatry 1988; 51: 745–752.
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Booij, J., Tissingh, G., Winogrodzka, A. et al. Practical benefit of [123I]FP-CIT SPET in the demonstration of the dopaminergic deficit in Parkinson's disease. Eur J Nucl Med 24, 68–71 (1997). https://doi.org/10.1007/BF01728311
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DOI: https://doi.org/10.1007/BF01728311