Advanced age is the major risk factor for idiopathic Parkinson’s disease (PD), but to date the biological relationship between PD and ageing remains elusive. Here we describe the rationale and the design of the H2020 funded project “PROPAG-AGEING”, whose aim is to characterize the contribution of the ageing process to PD development. We summarize current evidences that support the existence of a continuum between ageing and PD and justify the use of a Geroscience approach to study PD. We focus in particular on the role of inflammaging, the chronic, low-grade inflammation characteristic of elderly physiology, which can propagate and transmit both locally and systemically. We then describe PROPAG-AGEING design, which is based on the multi-omic characterization of peripheral samples from clinically characterized drug-naïve and advanced PD, PD discordant twins, healthy controls and "super-controls", i.e. centenarians, who never showed clinical signs of motor disability, and their offspring. Omic results are then validated in a large number of samples, including in vitro models of dopaminergic neurons and healthy siblings of PD patients, who are at higher risk of developing PD, with the final aim of identifying the molecular perturbations that can deviate the trajectories of healthy ageing towards PD development.

高龄是特发性帕金森病 (PD) 的主要危险因素，但迄今为止，PD 与衰老之间的生物学关系仍然难以捉摸。在这里，我们描述了 H2020 资助项目“PROPAG-AGEING”的基本原理和设计，该项目的目的是描述衰老过程对 PD 发展的贡献。我们总结了当前的证据，支持衰老和帕金森病之间存在连续性，并证明使用老年科学方法来研究帕金森病是合理的。我们特别关注炎症的作用，炎症是老年生理学的慢性、低度炎症特征，它可以局部和全身传播和传播。然后，我们描述了 PROPAG-AGEING 设计，该设计基于来自临床特征的未用药和晚期 PD、PD 不一致双胞胎、健康对照和“超级对照”（即从未表现出临床症状的百岁老人）的外周样本的多组学特征。运动障碍的迹象及其后代。然后在大量样本中验证组学结果，包括多巴胺能神经元的体外模型和帕金森病患者的健康兄弟姐妹，这些患者患帕金森病的风险较高，最终目的是确定可能偏离帕金森病轨迹的分子扰动。健康老龄化促进帕金森病的发展。