The Characteristics of Telomere length and Mitochondrial DNA from Peripheral Blood in Unsmoked Chinese Parkinson’s disease Patients

Introduction : Telomere length and mitochondrial DNA (mtDNA) biomarkers (mtDNA copy number and mtDNA common deletion) are considered to be involved in age-related disorders and neurodegenerative diseases. The relationship and potential mechanism between these three aging-biomarkers and Parkinson’s disease (PD) is not yet fully understood. Method : This study aimed to measure the peripheral blood leukocyte telomere length, mtDNA copy number and mtDNA common deletion by quantitative polymerase chain reaction in PD patients and healthy controls. A total number of 64 PD patients were recruited from the Department of Neurology, Beijing Xuanwu Hospital for this study, and 65 controls were recruited from the community cohort. All individuals are nonsmokers and underwent neuropsychological tests to assess cognitive function. All patients underwent Hoehn-Yahr stages and Movement Disorder Society Unified Parkinson’s Disease Rating Scale Part 2/3. Results : The result showed that there were no significant differences about these three aging biomarkers between the PD patients and controls. However, the spearman correlation analysis showed that the telomere length was negatively correlated with age (PD: p=0.007; Control: p=0.021) and positively correlated with mtDNA copy number both in PDs (p<0.001) and healthy controls (p=0.016). In PD group, mtDNA common deletion was positively correlated with age (p=0.001) and was also positively correlated with mtDNA copy number (p=0.023). Discussion : There is a potential interaction between the telomere length and mtDNA copy number in all population. However, telomere length and mtDNA biomarkers might not be used as the risk factor for PD. With the increase of age in PD, the cell senescence and the mitochondrial dysfunction are aggravated, and the mtDNA common deletion is overloaded. Meanwhile, the mtDNA copy number is also increased with the increased mtDNA commom deletion, which may be a compensatory mechanism to maintain the stability of mitochondrial function under PD pathological conditions.