MicroRNAs in Parkinson's disease and emerging therapeutic targets.

摘要: Parkinson's disease (PD) is the second most common age-related neurodegenerative disorder, with clinical main symptoms caused by a loss of dopaminergic neurons in substantia nigra, corpus striatum and brain cortex. Over 90% patients PD have sporadic occur people no known family history disorder. Currently there cure for PD. Treatment medications to increase dopamine relieves but does not slow down or reverse damage brain. Increasing evidence points inflammation as chief mediator inflammatory response mechanisms, involving microglia leukocytes, activated following neurons. Oxidative stress also recognized one causes PD, excessive reactive oxygen species (ROS) nitrogen can lead neuron vulnerability eventual death. MicroRNAs control range physiological pathological functions, may serve potential targets intervention against mitigate Several studies demonstrated that microRNAs regulate oxidative prevent ROS-mediated neurons, suggesting specific be putative novel therapeutic strategies Recent human animal identified large number dysregulated tissue samples, many which were downregulated. The affect downstream such SNCA, PARK2, LRRK2, TNFSF13B, LTA, SLC5A3, PSMB2, GSR, GBA, LAMP-2A, HSC. Apart from study, none reviewed had used agomirs antagomirs levels downregulated upregulated microRNAs, respectively, mouse models isolated cells. Further large-scale samples collected short postmortem interval are warranted provide more information on microRNA profiles different regions test gender differences.