A common pathological feature of neurodegenerative disorders (NDs), such as Alzheimer's (AD) and Parkinson's (PD) diseases, is the abnormal accumulation and misfolding of specific proteins, primarily α-synuclein (α-syn), β-amyloid1-42 (Aβ) and tau, in brain and in peripheral tissues too. Oxidative stress has been proved to be involved in NDs at various levels and, in particular, in such protein alterations, on the contrary physical activity is emerging as a counteracting factor in NDs. In the present work, the content of Aβ, α-syn and tau in red blood cells (RBCs) derived from ten endurance athletes (ATHL) and ten sedentary volunteers (SED) were compared before and after in vitrooxidative stress treatment. Total Aβ, α-syn and tau were quantified in RBCs (isolated from the subjects) by immunoenzymatic assays. Oxidative stress was induced by in vitro H₂O₂ administration to RBCs. H₂O₂ treatment was confirmed to significantly enhance ROS accumulation in RBCs. Total Aβ content in RBCs was lower in the ATHL subgroup with respect to the SED one. In the SED subgroup, but not in the ATHL one, total Aβ levels were increased by oxidative stress. Total α-syn content was lower in the ATHL subgroup with respect to the SED one and α-syn levels were increased by oxidative stress in both subgroups, with the percentage of increase higher in SED. Total tau content was comparable in both ATHL and SED and it was not affected by oxidative stress. Our data confirm previous findings evidencing that both oxidative stress and sedentary style contribute to aberrant folding and accumulation of NDs-related proteins, pointing to the importance of both anti-oxidant therapies and exercising in the prevention and treating of such diseases.

中文翻译：

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体育锻炼对β-淀粉样蛋白，α-突触核蛋白和tau积累的影响：人类红细胞氧化应激的体外模型。

神经退行性疾病（NDs）（例如阿尔茨海默氏病（AD）和帕金森氏病（PD）疾病）的常见病理特征是特定蛋白质（主要是α-突触核蛋白（α-syn），β-淀粉样蛋白1-42（ Aβ）和tau，也存在于大脑和周围组织中。已经证明氧化应激以各种水平参与ND，尤其是在这种蛋白质改变中，相反，身体活动正逐渐成为ND中的抵消因子。在目前的工作中，比较了体外氧化应激治疗前后来自十个耐力运动员（ATHL）和十个久坐的志愿者（SED）的红细胞（RBC）中Aβ，α-syn和tau的含量。通过免疫酶测定法对红细胞中的总Aβ，α-syn和tau进行定量（从受试者中分离）。通过向红细胞进行体外H 2 O 2诱导氧化应激。证实H 2 O 2处理能显着增强红细胞中ROS的积累。相对于SED，ATHL亚组中RBC中总Aβ含量较低。在SED亚组中，但在ATHL中没有，总Aβ水平由于氧化应激而增加。相对于SED，ATHL亚组的总α-syn含量较低，两个亚组中的氧化应激均使α-syn水平升高，而SED的升高百分比更高。总tau含量在ATHL和SED中均相当，并且不受氧化应激的影响。我们的数据证实了先前的发现，证明氧化应激和久坐的方式均会导致NDs相关蛋白的异常折叠和积累，