Mitochondrial Dysfunction Appears in the Hippocampal Neurons of 3-Month-Old Alpha-Synuclein Transgenic Mice
Author(s): Zegang Ma, Shang Liu
Alpha-synuclein A53T transgenic mouse (A53T) is an essential tool to investigate the onsets and the extents of Parkinson’s disease (PD) non-motor symptoms. Previous studies showed A53T mice exhibit a number of non-motor symptoms. However, the cause for these non-motor symptoms is still unknown. Our aim is to investigate the mitochondrial function in the hippocampal neurons of 3-month-old A53T mice. By enzyme-linked immunosorbent assay, we showed that the reactive oxidative species (ROS) level significantly increased in the hippocampus of A53T mice compared with that of the littermate controls. The cytochrome C content in the hippocampus of the A53T mice also increased. In addition, the ATP content decreased in the hippocampus of the A53T mice compared with the control. These results indicate that mitochondrial dysfunction appears in the hippocampal neurons of A53T mice, which may contribute to the cognitive disturbence in the young A53T mice.
Parkinson's disease, A53T, Non-Motor Symptoms, Mitochondrial Dysfunction
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International Journal of Sciences is Open Access Journal.
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