Role of Telomeres and Telomerase in Parkinson's Disease-A New Theranostics?
Balachandar VellingiriKiruthika BalasubramaniMahalaxmi IyerNeethu RajAjay ElangovanKwonwoo SongHan-Cheol YeoNamitha JayakumarMasako KinoshitaRavimanickam ThangarasuArul NarayanasamyAhmed Abdal DayemVijay Kumar PrajapatiAbilash Valsala GopalakrishnanSsang-Goo ChoPublished in: Advanced biology (2023)
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.
Keyphrases
- oxidative stress
- dna damage
- end stage renal disease
- ischemia reperfusion injury
- stem cells
- induced apoptosis
- newly diagnosed
- circulating tumor
- diabetic rats
- inflammatory response
- chronic kidney disease
- spinal cord
- cell free
- prognostic factors
- risk factors
- endoplasmic reticulum stress
- patient reported
- patient reported outcomes