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Targeting on calcium overload mediated brain aging and PD

Targeting on calcium overload mediated brain aging and PD

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中国神经科学学会第十二届全国学术会议

作者： Rong Cai Lei Liu Center of Stroke Beijing Institute for Brain Disorders Capital Medical University

Objective Brain aging associates with increasing intracellular calcium and decreasing brain energy. These two processes are likely correlated. For instance, calcium overload may trigger mitochondrial fragmentation which decreases its energy production. As a feedback, decreased energy output results in failure to maintain calcium gradients across the membrane and promotes calcium overload. Therefore, calcium overload and energy failure together may accelerate brain aging（accelerated aging hypothesis）. Our previous study demonstrated that miro/vimar complex served as a mediator of calcium overload and mitochondrial fragmentation. miro is a small GTPase, well known for its function to regulate mitochondrial morphology and transportation. vimar is the guanine nucleotide exchange factor of miro that we identified in Drosophila. The mammalian homolog of vimar is RAP1 GDS1. Methods To test the accelerated aging hypothesis, we generated transgenic flies to overload calcium and performed genetic manipulation on miro/vimar complex. In rodent Parkinson disease（PD） models, energy failure due to mitochondrial dysfunction has been well known to play a key pathophysiological role. Therefore, we select to target energy failure in PD to test the potential application of the hypothesis. To restore cellular energy, our previous study showed that terazosin（TZ） can activate glycolysis in vitro. Here, we tested whether TZ might act as a neuroprotective agent in rodent models of PD. Results 1) Calcium overload in the transgenic flies（overexpressed a leaky cation channel） reduced their locomotion ability, but no lifespan reduction, indicating calcium overload may enhance dementia in flies. 2) TZ could promote aerobic glycolysis and energy recovery in mouse brain in vivo. TZ showed strong rescue effects against the MPTP induced PD models in mice and the 6-OHDA induced PD model in rats. Conclusion Accelerated aging hypothesis is supported by our current results, but more work is still needed

关键词： Mitochondrial dysfunction Parkinson’s disease Energy failure Calcium overload Brain aging Terazosin Aerobic glycolysis miro/vimar Drosophila genetics

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