Gene Dysfunction Mediates Immune Response to Dopaminergic Degeneration in Parkinson's Disease.
Zhigang JiaoWenlong ZhangChaojun ChenXiaoqin ZhuXiang ChenMiaomiao ZhouGuoyou PengHanqun LiuJiewen QiuYuwan LinShuxuan HuangMingshu MoXinling YangShaogang QuPing-Yi XuPublished in: ACS chemical neuroscience (2018)
Many publications reported that genetic dysfunction mediates abnormal immune responses in the brain, which is important for the development of neurodegenerative diseases, especially for Parkinson's disease (PD). This immune disorder results in subsequent inflammatory reaction, which stimulates microglia or other immune cells to secrete cytokines and chemokines and disturbs the proportion of peripheral blood lymphocyte subsets contributing to dopaminergic (DA) neuron apoptosis. Furthermore, the abnormal immune related signal pathways caused by genetic variants promote chronic inflammation destroying the blood-brain barrier, which allows infiltration of different molecules and blood cells into the central nervous system (CNS) exerting toxicity on DA neurons. As a result, the inflammatory reaction in the CNS accelerates the progression of Parkinson's disease and promotes α-synuclein aggregation and diffusion among DA neurons in the procession of Parkinson's disease. Thus, for disease evaluation, the genetic mediated abnormal immune response in PD may be assessed based on the multiple immune molecules and inflammatory factors, as well as the ratio of lymphocyte subsets from PD patient's peripheral blood as potential biomarkers.
Keyphrases
- peripheral blood
- immune response
- oxidative stress
- genome wide
- cell cycle arrest
- dendritic cells
- spinal cord
- blood brain barrier
- cell death
- multiple sclerosis
- inflammatory response
- dna methylation
- cell proliferation
- spinal cord injury
- transcription factor
- white matter
- neuropathic pain
- drug induced
- genome wide analysis