Telomeres, which are repetitive sequences that cap the end of the chromosomes, shorten with each cell division. Besides cellular aging, there are several other factors that influence telomere length (TL), in particular, oxidative stress and inflammation, which play an important role in the pathogenesis of neurodegenerative brain diseases including Parkinson’s disease (PD). So far, the majority of studies have not demonstrated a significant difference in TL between PD patients and healthy individuals. However, studies investigating the effect of TL on the symptomatology and disease progression of PD are scarce, and thus, warranted. We analyzed TL of peripheral blood cells in a sample of 204 PD patients without concomitant autoimmune diseases and analyzed its association with several PD related phenotypes. Monochrome multiplex quantitative PCR (mmqPCR) was used to determine relative TL given as a ratio of the amount of DNA between the telomere and albumin as the housekeeping gene. We found a significant difference in the relative TL between PD patients with and without dementia, where shorter TL presented higher risk for dementia (p = 0.024). However, the correlation was not significant after adjustment for clinical factors (p = 0.509). We found no correlations between TLs and the dose of dopaminergic therapy when the analysis was adjusted for genetic variability in inflammatory or oxidative factors. In addition, TL influenced time to onset of motor complications after levodopa treatment initiation (p = 0.0134), but the association did not remain significant after adjustment for age at inclusion and disease duration (p = 0.0781). Based on the results of our study we conclude that TL contributes to certain PD-related phenotypes, although it may not have a major role in directing the course of the disease. Nevertheless, this expends currently limited knowledge regarding the association of the telomere attrition and the disease severity or motor complications in Parkinson’s disease.

中文翻译：

---

端粒长度的评估及其对帕金森氏病症状的影响

端粒是覆盖染色体末端的重复序列，随着每个细胞分裂而缩短。除了细胞衰老外，还有其他一些影响端粒长度（TL）的因素，特别是氧化应激和炎症，它们在包括帕金森氏病（PD）在内的神经变性脑疾病的发病机理中起着重要作用。到目前为止，大多数研究尚未证明PD患者与健康个体之间的TL有显着差异。但是，关于TL对PD的症状和疾病进展的影响的研究很少，因此有必要进行。我们分析了204例无伴随自身免疫性疾病的PD患者的外周血细胞TL，并分析了其与几种PD相关表型的相关性。单色多重定量PCR（mmqPCR）用于确定相对TL，相对TL以端粒和白蛋白之间的DNA量之比作为管家基因。我们发现患有和不患有痴呆的PD患者之间的相对TL有显着差异，其中TL越短表示痴呆的风险越高（p = 0.024）。但是，在校正临床因素后，相关性并不显着（p = 0.509）。当针对炎症或氧化因子的遗传变异性进行调整后，我们发现TL与多巴胺能治疗剂量之间没有相关性。此外，TL影响左旋多巴治疗开始后运动并发症发作的时间（p = 0.0134），但是在调整纳入年龄和疾病持续时间后，该关联性仍然不显着（p= 0.0781）。根据我们的研究结果，我们得出结论，尽管TL在指导疾病进程中可能没有主要作用，但它有助于某些PD相关的表型。然而，这花费了关于端粒损耗与帕金森氏病的疾病严重性或运动并发症的关联的当前有限的知识。