Department of Nuclear Medicine and PET, Aarhus University Hospital, Denmark.
Department of Nuclear Medicine and PET, Aarhus University Hospital, Denmark.
Parkinsonism Relat Disord. 2024 Oct;127:107117. doi: 10.1016/j.parkreldis.2024.107117. Epub 2024 Aug 30.
The a-Synuclein Origin and Connectome (SOC) model of Lewy body diseases postulates that a-syuclein will be asymmetrically distributed in some patients with Lewy body diseases, potentially leading to asymmetric neuronal dysfunction and symptoms.
We included two patient groups: 19 non-demented Parkinson's disease (nPD) patients with [F]FDG PET and motor symptoms assessed by UPDRS-III, and 65 Lewy body dementia (LBD) patients with [F]FDG PET and dopamine radioisotope imaging. Asymmetry indices were calculated for [F]FDG PET by including the cortex for each hemisphere, for dopamine radioisotope imaging by including the putamen and caudate separately, and for motor symptoms by using the difference between right-left UPDRS-III score. Correlations between these asymmetry indices were explored to test the predictions of the SOC model. To identify cases with a more typical LBD imaging profile, we calculated a Cingulate Island Sign (CIS) index on the [F]FDG PET image.
We found a significant correlation between cortical interhemispheric [F]FDG asymmetry and motor-symptom asymmetry in nPD patients (r = 0.62, P = 0.004). In patients with LBD, we found a significant correlation between cortical interhemispheric [F]FDG asymmetry and dopamine transporter asymmetry in the caudate (r = 0.37, P = 0.0019), but not in the putamen (r = 0.15, P = 0.22). We observed that the correlation in the caudate was stronger in LBD subjects with the highest CIS index, i.e., with more typical LBD imaging profiles.
Our study partly supports the SOC model, but further investigations are needed - ideally of de novo, non-demented PD patients.
路易体病的α-突触核蛋白起源和连接组（SOC）模型假设，在一些路易体病患者中，α-突触核蛋白将呈现不对称分布，这可能导致不对称的神经元功能障碍和症状。
我们纳入了两个患者组：19 名非痴呆帕金森病（nPD）患者，进行了[F]FDG PET 和 UPDRS-III 评估的运动症状，以及 65 名路易体痴呆（LBD）患者，进行了[F]FDG PET 和多巴胺放射性同位素成像。通过包括每个半球的皮层，为[F]FDG PET 计算不对称指数，通过分别包括壳核和尾状核，为多巴胺放射性同位素成像计算不对称指数，以及通过使用右-左 UPDRS-III 评分之间的差异来计算运动症状的不对称指数。为了检验 SOC 模型的预测，我们探索了这些不对称指数之间的相关性。为了识别更典型的 LBD 成像特征的病例，我们在[F]FDG PET 图像上计算了一个扣带岛标志（CIS）指数。
我们发现 nPD 患者中皮层半球间[F]FDG 不对称与运动症状不对称之间存在显著相关性（r=0.62，P=0.004）。在 LBD 患者中，我们发现皮层半球间[F]FDG 不对称与尾状核多巴胺转运体不对称之间存在显著相关性（r=0.37，P=0.0019），但在壳核中无显著相关性（r=0.15，P=0.22）。我们观察到，在具有最高 CIS 指数的 LBD 受试者中，尾状核的相关性更强，即具有更典型的 LBD 成像特征。
我们的研究部分支持 SOC 模型，但需要进一步的研究-理想情况下是对首发、非痴呆性 PD 患者进行研究。
