帕金森病新皮质单胺末端的PET成像。

R M Marié, L Barré, P Rioux, P Allain, B Lechevalier, J C Baron
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引用次数: 53

摘要

帕金森病(PD)的死后神经化学研究表明,除了典型的黑质纹状体多巴胺脱神经外,还存在伴随的新皮质单胺纤维脱神经(严重程度不同),其在运动,特别是相关的认知和情感障碍中的作用尚不清楚。11c - s -诺米芬(11C-NMF)是多巴胺和去甲肾上腺素突触前再摄取位点的放射性配体,目前已用于纹状体的研究,我们已经广泛研究了11c - s - nmf的PET成像是否可以提供一种评估PD患者体内新皮质单胺末端损失的方法;以前,这是一个很少被提及和有争议的问题。为此,我们前瞻性地选择了一个高度均匀的样本,包括9名非痴呆、非抑郁的特发性PD患者,这些患者在运动损伤方面有轻微到明显的侧对侧不对称性。除了恢复先前报道的与壳层11C-NMF特异性摄取不对称的相关性外,临床运动不对称也与新皮层(特别是额叶)11C-NMF不对称在临床预期的方向上显著相关,这表明单胺类新皮层去神经控制可能在PD的运动损伤中起直接作用。这些结果表明,有可能在体内评估新皮质单胺末端丧失,并阐明其在帕金森病和非典型退行性帕金森病中复杂认知和情感障碍中的潜在作用。
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PET imaging of neocortical monoaminergic terminals in Parkinson's disease.

Post-mortem neurochemical studies in Parkinson's disease (PD) have shown that, in addition to the typical nigro-striatal dopamine denervation, there exists a concomitant neocortical monoamine fibre deafferentation (of variable severity) whose role in motor, and especially in associated cognitive and affective impairment, remains elusive. We have extensively examined whether PET imaging with 11C-S-Nomifensine (11C-NMF), a radioligand of the dopamine and norepinephrine presynaptic reuptake sites which has been used so far to investigate the striatum, could provide a method for assessing in vivo the neocortical monoamine terminal loss in PD; previously, this has been a little addressed and controversial issue. To this end, we prospectively selected a highly homogeneous sample of nine non-demented, non-depressed idiopathic PD patients with mild to marked side-to-side asymmetry in motor impairment. In addition to recovering the previously-reported correlations with putaminal 11C-NMF specific uptake asymmetries, the clinical motor asymmetries also significantly correlated in the clinically expected direction to neocortical (especially frontal) 11C-NMF asymmetries, suggesting the monoamine neocortical denervation might play a direct role in motor impairment in PD. These results demonstrate that it is possible to assess in vivo the neocortical monoamine terminal loss, and to elucidate its potential role in the complex cognitive and affective impairment, in both PD and atypical degenerative parkinsonism.

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Fibroblast growth factors: structure-activity on dopamine neurons in vitro. Injection of a minuscule dose of FeCl3 within the ventrolateral striatum causes a chronic disturbance of the integrative function within the limbic part of the ventral striatum. Locomotor effects of amantadine in the mouse are not those of a typical glutamate antagonist. Markers of dopamine depletion and compensatory response in striatum and cerebrospinal fluid. PET imaging of neocortical monoaminergic terminals in Parkinson's disease.
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