PDF(Pubmed)
Abstract：
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.
摘要：
有人建议饮酒可以预防帕金森氏病（PD）。在这里，我们评估了100名死亡年龄在51至93岁之间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脑和肝脏病理（LP）。我们的队列包括没有受试者，温和,中度,和严重的LP引起的饮酒。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，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。观察到的阿尔茨海默氏II型星形胶质细胞与大脑中的αS病理之间存在显着负相关。LP和过度磷酸化τ（HPτ）之间没有发现关联。LP的程度与HPτ的程度之间没有显着相关性，大脑中的淀粉样β蛋白（Aβ）或反式DNA结合蛋白43（TDP43）。在HPτ的程度之间观察到显着的相关性，Aβ,αS,和TDP43在大脑和肝脏脂肪变性之间，炎症,和纤维化。患有严重LP的受试者表现出更高的阿尔茨海默氏症II型星形胶质细胞频率，或温和，LP.评估的蛋白质改变在患有阿尔茨海默氏症II型星形胶质细胞的受试者中并不更普遍或更严重。在所有情况下,痴呆症归因于蛋白质改变的组合，即，轻度LP患者中有30％观察到痴呆和痴呆的混合性，而重度LP患者中有13％观察到。总之,我们的结果与最近两项荟萃分析的结果一致,这些荟萃分析提示有饮酒史的受试者很少发生α-突触核蛋白病.
