Protective effect of α-synuclein knockdown on dopaminergic neurons

The over-expression of α-synuclein is a major factor in the death of dopaminergic neurons in a methamphetamine-induced model of Parkinson's disease (PD).

Dr. Huijun Wang, School of Basic Medical Sciences, Southern Medical University, China and his team injected α-synuclein-shRNA lentivirus stereotaxically into the right striatum of experimental rats to inhibit α-synuclein mRNA and protein expression. Results showed that after α-synuclein knockdown, the depression manifestations of PD rats were reduced, striatal dopamine and tyrosine hydroxylase levels as well as superoxide dismutase activity were significantly increased, but the levels of reactive oxygen species, malondialdehyde, nitric oxide synthase and nitrogen monoxide were decreased, and simultaneously, the number of apoptotic cells in the striatum was significantly decreased. The authors considered α-synuclein has the capacity to reverse methamphetamine-induced apoptosis of dopaminergic neurons in the rat striatum by inhibiting oxidative stress and improving dopaminergic system function.

Related results were published in NeuralRegeneration Research (Vol. 9, No. 9, 2014).

More information:
Tai YC, Chen L, Huang EP, Liu C, Yang XY, Qiu PM, Wang HJ. Protective effect of alpha-synuclein knockdown on methamphetamine-induced neurotoxicity in dopaminergic neurons. Neural Regen Res. 2014;9(9):951-958.

Provided by Neural Regeneration Research