In vivo molecular neuroimaging for motor or cognitive dysfunction in non-human primate model of Parkinson's disease

帕金森病非人灵长类动物模型运动或认知功能障碍的体内分子神经影像学

• 批准号: 21791229
• 负责人: NAGAI Yuji
• 金额: $ 2.83万
• 依托单位: National Institute of Radiological Sciences
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21791229/
• 关键词: 核医学(PETを含む); パーキンソン病; 高次脳機能障害; ポジトロンCT; トランスレーショナルリサーチ; トランスルーショナルリサーチ

Repeated MPTP-treated monkeys were examined relationship between motor or cognitive function and dopaminergic function by PET. Motor activity was significantly correlated with dopamine transporter binding specifically in the ventrolateral putamen, which corresponds to the area receiving motor inputs from the primary motor cortex. These results suggested that specific functional deficits in PD models were caused by degeneration of dopaminergic terminals in the striatal subregion responsible for that function in a manner dependent on the degree of degeneration.

通过PET检查重复MPTP治疗的猴子的运动或认知功能与多巴胺能功能之间的关系。运动活动显着相关，多巴胺转运蛋白结合特异性腹外侧壳核，这对应于该地区接受运动输入的初级运动皮层。这些结果表明，PD模型中的特定功能缺陷是由纹状体亚区中负责该功能的多巴胺能末梢以依赖于变性程度的方式变性引起的。