端粒
端粒酶
外周血单个核细胞
生物标志物
氧化应激
人口
疾病
癌症研究
生物
医学
免疫学
DNA
基因
遗传学
病理
内科学
环境卫生
体外
作者
Balachandar Vellingiri,Kiruthika Balasubramani,Mahalaxmi Iyer,Neethu Raj,Ajay Elangovan,Kwonwoo Song,H. Yeo,N. Jayakumar,Masako Kinoshita,Ravimanickam Thangarasu,Arul Narayanasamy,Ahmed Abdal Dayem,Vijay Kumar Prajapati,Abilash Valsala Gopalakrishnan,Ssang‐Goo Cho
标识
DOI:10.1002/adbi.202300097
摘要
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.
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