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The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease
Published on: October 3, 2012
Genetic predisposition to Parkinson's disease and cancer
Zhiming Li, Qing Lin, Qilin Ma
1School of Pharmaceutical Sciences, Xiamen University, Xiamen 361005, Fujian, China. cmtzeng@xmu.edu.cn.
Abstract:
Parkinson's disease (PD) and cancer are often thought of as two sides of the same coin. At first glance, cancer and PD appear to have little in common. PD is caused by the degeneration of dopaminergic neurons, whereas cancer results from the uninhibited growth of tumor cells. Increasing numbers of genetic studies suggest that the pathogenesis of PD and cancer may involve similar genes, pathways, and mechanisms. The differences in the pathological and cellular mechanisms, and the associated genetic mutations, may result in two such divergent diseases. In this article, we highlight some molecular mechanisms and key biomarkers which might cause those two diseases from misfolding and degradation of proteins, mitochondrial damage, oxidative stress response, cell cycle control and DNA repair, and the PI3K/AKT/ mTOR pathway, in order to provide help to the understanding and treatment of these two diseases.
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