2007
DOI: 10.1002/mds.21315
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Higher nigrostriatal dopamine neuron loss in early than late onset Parkinson's disease?—A [99mTc]‐TRODAT‐1 SPECT study

Abstract: Early-onset Parkinson's disease (EOPD) is distinct from the classic late-onset PD (LOPD) because of its slower disease progression. The aim of this study was to compare dopamine neuronal loss in EOPD with that of LOPD with the same disease duration, through dopamine transporter (DAT) estimation. Fourteen patients, seven EOPD (<50 years) and seven LOPD, matched for disease duration were scanned with [(99m)Tc]-TRODAT-1-SPECT (INER-Taiwan), and were assessed with standard PD scales. EOPD patients had 34% lower st… Show more

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Cited by 57 publications
(49 citation statements)
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References 14 publications
(16 reference statements)
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“…In both single-and dual-isotope SPECT using [ 99m Tc]TRO-DAT-1 as one of the ligands, its uptake at 210-240 min postinjection in a 6-OHDA-lesioned PD Formosan rock monkey was 39% of the uptake seen at the same postinjection time in control monkeys [22]. In humans, its uptake is lower in patients with PD than in those with multiple system atrophy [24], and its uptake decreases as PD severity increases [16,[25][26][27]. The results of this simultaneous dual-isotope SPECT approach also reaffirm a lowaffinity binding of [ 99m Tc]TRODAT-1 to SERT that persists even after pretreatment with fluoxetine.…”
Section: Discussionmentioning
confidence: 99%
“…In both single-and dual-isotope SPECT using [ 99m Tc]TRO-DAT-1 as one of the ligands, its uptake at 210-240 min postinjection in a 6-OHDA-lesioned PD Formosan rock monkey was 39% of the uptake seen at the same postinjection time in control monkeys [22]. In humans, its uptake is lower in patients with PD than in those with multiple system atrophy [24], and its uptake decreases as PD severity increases [16,[25][26][27]. The results of this simultaneous dual-isotope SPECT approach also reaffirm a lowaffinity binding of [ 99m Tc]TRODAT-1 to SERT that persists even after pretreatment with fluoxetine.…”
Section: Discussionmentioning
confidence: 99%
“…SAD may be a psychosocial reaction to the stigmatizing PD symptoms such as tremor and bradykinesia, but abnormal function of the striatum has been pointed as one of the key pathophysiological mechanism implicated in SAD [20][21][22][23] and it is also plausible that the profound disruption of the main catecholaminergic and serotonergic pathways that occurs in PD 24 predispose patients to SAD. In our sample, SAD was associated with the intensity of motor symptoms, younger age and with earlier age at disease onset, all of which imply both in higher psychosocial stress and in more severe nigrostriatal dopaminergic denervation 25,26 .…”
Section: Discussionmentioning
confidence: 63%
“…In addition to provide earlier diagnosis and lesion identification, they provide assessment of presynaptic and postsynaptic nigrostriatal dopaminergic pathways that cannot be achieved with MRI [10][11][12]. Of particular interest, in this case presynaptic ( 99m T C -TRO-DAT-1) and postsynaptic ( 123 I-IBZM) imaging provided a complete picture of the nigrostriatal dopaminergic pathway.…”
Section: Discussionmentioning
confidence: 99%