Stem Cell and Regenerative Medicine/Translational Research, Department of Zoology, School of Basic Sciences, Central University of Punjab, Bathinda, Punjab, 151401, India.
Human Molecular Cytogenetics and Stem Cell Laboratory, Department of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Tamil Nadu, 641046, India.
Adv Biol (Weinh). 2023 Dec;7(12):e2300097. doi: 10.1002/adbi.202300097. Epub 2023 Aug 17.
Parkinson's disease (PD) is a complex condition that is significantly influenced by oxidative stress and inflammation. It is also suggested that telomere shortening (TS) is regulated by oxidative stress which leads to various diseases including age-related neurodegenerative diseases like PD. Thus, it is anticipated that PD would result in TS of peripheral blood mononuclear cells (PBMCs). Telomeres protect the ends of eukaryotic chromosomes preserving them against fusion and destruction. The TS is a normal process because DNA polymerase is unable to replicate the linear ends of the DNA due to end replication complications and telomerase activity in various cell types counteracts this process. PD is usually observed in the aged population and progresses over time therefore, disparities among telomere length in PBMCs of PD patients are recorded and it is still a question whether it has any useful role. Here, the likelihood of telomere attrition in PD and its implications concerning microglia activation, ageing, oxidative stress, and the significance of telomerase activators are addressed. Also, the possibility of telomeres and telomerase as a diagnostic and therapeutic biomarker in PD is discussed.
帕金森病(PD)是一种复杂的疾病,其发病机制受氧化应激和炎症的显著影响。有研究表明,端粒缩短(TS)受氧化应激调节,而氧化应激会导致各种疾病,包括与年龄相关的神经退行性疾病,如 PD。因此,预计 PD 会导致外周血单核细胞(PBMC)的 TS。端粒保护真核染色体的末端,防止其融合和破坏。TS 是一个正常的过程,因为由于末端复制的复杂性,DNA 聚合酶无法复制 DNA 的线性末端,而各种细胞类型中的端粒酶活性会对抗这个过程。PD 通常发生在老年人群中,并随时间推移而进展,因此,PD 患者 PBMC 中端粒长度的差异被记录下来,端粒是否具有任何有用的作用仍然是一个问题。在这里,我们将讨论 PD 中端粒损耗的可能性及其对小胶质细胞激活、衰老、氧化应激的影响,以及端粒酶激活剂的重要性。此外,还讨论了端粒和端粒酶作为 PD 诊断和治疗生物标志物的可能性。