遗传帕金森病中的多巴胺能神经元成像：发病机制的新见解。
Dopaminergic neuronal imaging in genetic Parkinson's disease: insights into pathogenesis.
机构信息
Department of Clinical Neurosciences, Institute of Neurology, University College London, London, United Kingdom.
出版信息
PLoS One. 2013 Jul 23;8(7):e69190. doi: 10.1371/journal.pone.0069190. Print 2013.
OBJECTIVES
To compare the dopaminergic neuronal imaging features of different subtypes of genetic Parkinson's Disease.
METHODS
A retrospective study of genetic Parkinson's diseases cases in which DaTSCAN (123I-FP-CIT) had been performed. Specific non-displaceable binding was calculated for bilateral caudate and putamen for each case. The right:left asymmetry index and striatal asymmetry index was calculated.
RESULTS
Scans were available from 37 cases of monogenetic Parkinson's disease (7 glucocerebrosidase (GBA) mutations, 8 alpha-synuclein, 3 LRRK2, 7 PINK1, 12 Parkin). The asymmetry of radioligand uptake for Parkinson's disease with GBA or LRRK2 mutations was greater than that for Parkinson's disease with alpha synuclein, PINK1 or Parkin mutations.
CONCLUSIONS
The asymmetry of radioligand uptake in Parkinsons disease associated with GBA or LRRK2 mutations suggests that interactions with additional genetic or environmental factors may be associated with dopaminergic neuronal loss.
目的
比较不同遗传型帕金森病亚型的多巴胺能神经元成像特征。
方法
对已行 DaTSCAN（123I-FP-CIT）检查的遗传型帕金森病病例进行回顾性研究。为每个病例计算双侧尾状核和壳核的特定非置换性结合。计算右侧/左侧不对称指数和纹状体不对称指数。
结果
共获得 37 例单基因帕金森病（7 例葡萄糖脑苷脂酶（GBA）突变，8 例α-突触核蛋白，3 例 LRRK2，7 例 PINK1，12 例 Parkin）的扫描结果。GBA 或 LRRK2 突变相关帕金森病的放射性配体摄取不对称性大于α-突触核蛋白、PINK1 或 Parkin 突变相关帕金森病。
结论
与 GBA 或 LRRK2 突变相关帕金森病的放射性配体摄取不对称性表明，与其他遗传或环境因素的相互作用可能与多巴胺能神经元丢失有关。
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