Objective

To investigate the relationship of synaptic loss with glucose metabolism and dopaminergic transporters in Parkinson’s disease (PD) patients.

Methods

A total of 16 patients with PD and 11 age-matched healthy controls underwent positron emission tomography (PET) with the tracers [¹⁸F]SynVesT-1, a ligand for the presynaptic terminal marker synaptic vesicle protein 2 A (SV2A), and FDG. PD patients also underwent PET with the dopamine transporter (DAT) ligand [18F]FP-CIT. The difference in synaptic density between PD patients and age-matched normal controls(NCs) was determined in the selected regions of interest, and the correlations of the [¹⁸F]SynVesT-1 PET SUVRs with [¹⁸F]FP-CIT PET SUVRs and [¹⁸F]FDG PET SUVRs were evaluated.

Results

Compared with that in the NC group, the synaptic density in the caudate region was significantly lower in the PD group (SUVR: 2.51 ± 0.36 vs. 3.18 ± 0.32, p < 0.001), especially in the pre-commissural caudate and post-commissural caudate (SUVR: 2.42 ± 0.29 vs. 2.63 ± 0.32, p < 0.01; 0.76 ± 0.31 vs. 0.97 ± 0.33, p < 0.001). A reduced synaptic density was significantly correlated with DAT (r = 0.61, p < 0.001) and glucose metabolism (r = 0.73, p < 0.001) in the post-commissural caudate. In the post-commissural regions of the caudate, there was a partial mediating effect of synaptic density on the relationship between glucose metabolism and DAT availability (indirect effect: β₄ = 0.039, p = 0.024).

Conclusion

[¹⁸F]SynVesT-1 binds specifically to SV2A, reflecting synaptic density, and there is a positive correlation metabolic pattern related to the changes reflected by [¹⁸F]SynVesT-1 and [¹⁸F]FDG.

中文翻译：

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帕金森病患者的突触前末梢完整性与葡萄糖代谢有关

 目的

探讨帕金森病 （PD） 患者突触丢失与葡萄糖代谢和多巴胺能转运蛋白的关系。

 方法

共有 16 名 PD 患者和 11 名年龄匹配的健康对照者接受了示踪剂 [¹⁸F]SynVesT-1 的正电子发射断层扫描 （PET），示踪剂是突触前末端标志物突触囊泡蛋白 2 A （SV2A） 和 FDG 的配体。PD 患者还接受了多巴胺转运蛋白 （DAT） 配体 [18F]FP-CIT 的 PET。在选定的感兴趣区域确定 PD 患者与年龄匹配的正常对照 （NCs） 之间的突触密度差异，并评估 [¹⁸F]SynVesT-1 PET SUVRs 与 [¹⁸F]FP-CIT PET SUVRs 和 [¹⁸F]FDG PET SUVRs 的相关性。

 结果

与 NC 组相比，PD 组尾状核区的突触密度显著降低（SUVR：2.51 ± 0.36 vs. 3.18 ± 0.32，p < 0.001），尤其是在尾状结前尾状 核和尾状结后（SUVR：2.42 ± 0.29 对 2.63 ± 0.32，p < 0.01;0.76 ± 0.31 对 0.97 ± 0.33，p < 0.001）。 突触密度降低与尾状核后 DAT （r = 0.61，p % 3C 0.001） 和葡萄糖代谢 （r = 0.73，p < 0.001） 显著相关。 在尾状核的连合后区域，突触密度对葡萄糖代谢和 DAT 可用性之间的关系存在部分介导作用 （间接效应： β₄ = 0.039，p = 0.024）。

 结论

[¹⁸个地址]SynVesT-1 与 SV2A 特异性结合，反映突触密度，并且与 [¹⁸F]SynVesT-1 和 [¹⁸F]FDG 反映的变化呈正相关代谢模式。