Upregulation of APAF1 and CSF1R in Peripheral Blood Mononuclear Cells of Parkinson's Disease.
Kuo-Hsuan ChangChia-Hsin LiuYi-Ru WangYen-Shi LoChun-Wei ChangHsiu-Chuan WuChiung-Mei ChenPublished in: International journal of molecular sciences (2023)
Increased oxidative stress and neuroinflammation play a crucial role in the pathogenesis of Parkinson's disease (PD). In this study, the expression levels of 52 genes related to oxidative stress and inflammation were measured in peripheral blood mononuclear cells of the discovery cohort including 48 PD patients and 25 healthy controls. Four genes, including ALDH1A , APAF1 , CR1 , and CSF1R , were found to be upregulated in PD patients. The expression patterns of these genes were validated in a second cohort of 101 PD patients and 61 healthy controls. The results confirmed the upregulation of APAF1 (PD: 0.34 ± 0.18, control: 0.26 ± 0.11, p < 0.001) and CSF1R (PD: 0.38 ± 0.12, control: 0.33 ± 0.10, p = 0.005) in PD patients. The expression level of APAF1 was correlated with the scores of the Unified Parkinson's Disease Rating Scale (UPDRS, r = 0.235, p = 0.018) and 39-item PD questionnaire (PDQ-39, r = 0.250, p = 0.012). The expression level of CSF1R was negatively correlated with the scores of the mini-mental status examination (MMSE, r = -0.200, p = 0.047) and Montréal Cognitive Assessment (MoCA, r = -0.226, p = 0.023). These results highly suggest that oxidative stress biomarkers in peripheral blood may be useful in monitoring the progression of motor disabilities and cognitive decline in PD patients.
Keyphrases
- end stage renal disease
- oxidative stress
- poor prognosis
- ejection fraction
- chronic kidney disease
- newly diagnosed
- peritoneal dialysis
- prognostic factors
- cognitive decline
- cell proliferation
- small molecule
- mild cognitive impairment
- dna damage
- long non coding rna
- gene expression
- peripheral blood
- mental health
- ischemia reperfusion injury
- brain injury
- cerebrospinal fluid
- cognitive impairment
- genome wide identification
- binding protein