It has been suggested that alcohol consumption protects against Parkinson's disease (PD). Here we assessed postmortem tissue samples from the brains and livers of 100 subjects with ages at death ranging from 51 to 93. Twenty percent of these subjects were demented. We used standardized assessment strategies to assess both the brain and liver pathologies (LP). Our cohort included subjects with none, mild, moderate, and severe LP caused by alcohol consumption. We noted a significant negative correlation of categorical data between liver steatosis and α-synuclein (αS) in the brain and a significant negative correlation between the extent of liver steatosis and fibrosis and the extent of αS in the brain. There was a significant negative association between the observation of Alzheimer’s type II astrocytes and αS pathology in the brain. No association was noted between LP and hyperphosphorylated τ (HPτ). No significant correlation could be seen between the extent of LP and the extent of HPτ, amyloid β protein (Aβ) or transactive DNA binding protein 43 (TDP43) in the brain. There were significant correlations observed between the extent of HPτ, Aβ, αS, and TDP43 in the brain and between liver steatosis, inflammation, and fibrosis. Subjects with severe LP displayed a higher frequency of Alzheimer’s type II astrocytes compared to those with no, or mild, LP. The assessed protein alterations were not more prevalent or severe in subjects with Alzheimer’s type II astrocytes in the brain. In all cases, dementia was attributed to a combination of altered proteins, i.e., mixed dementia and dementia was observed in 30% of those with mild LP when compared with 13% of those with severe LP. In summary, our results are in line with the outcome obtained by the two recent meta-analyses suggesting that subjects with a history of alcohol consumption seldom develop an α-synucleinopathy.

有人建议饮酒可以预防帕金森病（PD）。在这里，我们评估了 100 名死亡年龄从 51 岁到 93 岁不等的受试者的大脑和肝脏的死后组织样本。这些受试者中有 20% 患有痴呆症。我们使用标准化评估策略来评估大脑和肝脏病理（LP）。我们的队列包括没有、轻度、中度和重度因饮酒引起的 LP 的受试者。我们注意到肝脏脂肪变性和大脑中 α-突触核蛋白 (αS) 之间的分类数据存在显着负相关，并且肝脏脂肪变性和纤维化的程度与大脑中 αS 的程度之间存在显着负相关。阿尔茨海默病 II 型星形胶质细胞的观察结果与大脑中的 αS 病理学之间存在显着的负相关。未发现 LP 与过度磷酸化 τ (HPτ) 之间存在关联。 LP 的程度与大脑中 HPτ、β 淀粉样蛋白 (Aβ) 或反式 DNA 结合蛋白 43 (TDP43) 的程度之间没有发现显着相关性。大脑中 HPτ、Aβ、αS 和 TDP43 的程度与肝脏脂肪变性、炎症和纤维化之间存在显着相关性。与没有或轻度腰椎间盘突出的受试者相比，患有严重腰椎间盘突出的受试者显示阿尔茨海默病 II 型星形胶质细胞的频率更高。在大脑中患有阿尔茨海默病 II 型星形胶质细胞的受试者中，所评估的蛋白质改变并不更普遍或更严重。在所有病例中，痴呆症均归因于蛋白质改变的组合，即，30% 的轻度 LP 患者出现混合性痴呆，而重度 LP 患者的这一比例为 13%。 总之，我们的结果与最近两项荟萃分析的结果一致，表明有饮酒史的受试者很少出现 α-突触核蛋白病。