A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Extrastriatal dopamine D-2 receptors in Parkinson's disease: a longitudinal study
Tekijät: Kaasinen V, Aalto S, Nagren K, Hietala J, Sonninen P, Rinne JO
Kustantaja: SPRINGER-VERLAG WIEN
Julkaisuvuosi: 2003
Journal: Journal of Neural Transmission
Tietokannassa oleva lehden nimi: JOURNAL OF NEURAL TRANSMISSION
Lehden akronyymi: J NEURAL TRANSM
Vuosikerta: 110
Numero: 6
Aloitussivu: 591
Lopetussivu: 601
Sivujen määrä: 11
ISSN: 0300-9564
DOI: https://doi.org/10.1007/s00702-003-0816-x
Tiivistelmä
Most antiparkinsonian drugs are known to act through central dopamine D-2 receptor agonism. A previous longitudinal positron emission tomography (PET) study has indicated that, in the striatum of Parkinson's disease (PD) patients, dopamine D-2 receptor binding declines at a relatively fast annual rate of 2-4% (compared to the rate of < 1%/year in healthy individuals). In the present study, the examination of longitudinal changes in D-2 receptors was extended to extrastriatal brain regions in PD. Eight early PD patients were examined twice with PET, similar to3 years apart, using a high-affinity extrastriatal D-2/D-3 receptor tracer, [C-11]FLB 457. Both the MRI-referenced region-of-interest method and the voxel-based statistical analysis method were used independently in the analysis. Regional D-2-like availabilities (binding potentials) in the left dorsolateral prefrontal cortex, the left temporal cortex and the left and right medial thalami were significantly decreased at the second examination by 20-37% (corresponding to an annual decline of 6-11%). Thus, the annual loss of extrastriatal D-2 availability in PD is up to three times faster than the rate previously reported in the putamen. Our longitudinal study shows first evidence concerning cortical D-2 receptor loss in the progression of PD, although it is not possible to distinguish between the effects of the therapy and the disease.
Most antiparkinsonian drugs are known to act through central dopamine D-2 receptor agonism. A previous longitudinal positron emission tomography (PET) study has indicated that, in the striatum of Parkinson's disease (PD) patients, dopamine D-2 receptor binding declines at a relatively fast annual rate of 2-4% (compared to the rate of < 1%/year in healthy individuals). In the present study, the examination of longitudinal changes in D-2 receptors was extended to extrastriatal brain regions in PD. Eight early PD patients were examined twice with PET, similar to3 years apart, using a high-affinity extrastriatal D-2/D-3 receptor tracer, [C-11]FLB 457. Both the MRI-referenced region-of-interest method and the voxel-based statistical analysis method were used independently in the analysis. Regional D-2-like availabilities (binding potentials) in the left dorsolateral prefrontal cortex, the left temporal cortex and the left and right medial thalami were significantly decreased at the second examination by 20-37% (corresponding to an annual decline of 6-11%). Thus, the annual loss of extrastriatal D-2 availability in PD is up to three times faster than the rate previously reported in the putamen. Our longitudinal study shows first evidence concerning cortical D-2 receptor loss in the progression of PD, although it is not possible to distinguish between the effects of the therapy and the disease.
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