Presynaptic terminal integrity is associated with glucose metabolism in Parkinson's disease.

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]SynVe...

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Publicado en:European Journal of Nuclear Medicine & Molecular Imaging Vol. 52; no. 4; pp. 1510 - 1520
Autores principales: Wang, Weiyi, Wang, Yanru, Xu, Limin, Liu, Xueling, Hu, Yuqing, Li, Junpeng, Huang, Qi, Ren, Shuhua, Huang, Yiyun, Guan, Yihui, Li, Yuxin, Hua, Fengchun, Ye, Qing, Xie, Fang
Formato: Journal Article
Publicado: Springer Nature Mar2025
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Mar2025
      vid: 52
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      pub: Springer Nature
      place: New York, New York
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        183131167
        181006011
        10.1007/s00259-024-06993-3
        183131167
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        atl: Presynaptic terminal integrity is associated with glucose metabolism in Parkinson's disease.
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          Wang, Weiyi
          Wang, Yanru
          Xu, Limin
          Liu, Xueling
          Hu, Yuqing
          Li, Junpeng
          Huang, Qi
          Ren, Shuhua
          Huang, Yiyun
          Guan, Yihui
          Li, Yuxin
          Hua, Fengchun
          Ye, Qing
          Xie, Fang
        affil: https://ror.org/013q1eq08 Department of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, 200040, Shanghai, China
      sug:
      ab: 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.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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