Role of Telomeres and Telomerase in Parkinson's Disease—A New Theranostics?

Abstract

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.

The Role of Glia Telomere Dysfunction in the Pathogenesis of Central Nervous System Diseases

“…A study conducted by Scheffold et al in a PD mouse model with telomere shortening phenotype (TERC knockout) indicated that earlier onset of synuclein aggregation had taken place with documented defective microglial immune response in the aged brain [ 39 ]. Thus, the study introduces the contribution of microglia telomere attrition in PD pathogenesis and adds to the hypothesis that telomere erosion with aging may be a risk factor in neurodegenerative disorders [ 40 ].…”