Abstract
Alzheimer’s disease (AD), the most common form of senile dementia, is associated with neurodegeneration. The development of Alzheimer’s disease is related to abnormalities of cell cycle regulation. Preliminary work showed that a novel gene, CAC1, was highly expressed in tumors and had an oncogene-like function related to cell cycle regulation. The pathogenesis of AD is still incompletely understood. In this study, we measured the expression level of CAC1 in the hippocampus of AD patients to explore the involvement of CAC1 in the development of AD. Our findings showed that the expression level of CAC1 in the hippocampus of AD patients was significantly lower than that of normal controls. The reduction of CAC1 expression did not affect tau/p-tau-396, amyloid precursor protein or apolipoprotein E4 in the in vitro model. A reduction of cyclin E was detected after a CAC1-knockdown. Interestingly, we found that the knockdown of CAC1 by RNAi led to an increase in oxidative stress and the level of p53 protein in SHSY-5Y cells. The expression of CAC1 in SHSY-5Y cells protected the cells from apoptosis induced by Aβ toxicity or oxidative stress. These results established that CAC1 is an important factor for the protection of cells against Aβ toxicity and oxidative stress.
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Acknowledgments
We appreciate the work of American Journal Experts (AJE) in the correction of the English text. This work was supported by funds from the National Natural Science Foundation of China (81000865), the science and technology projects of Xi'an city (SF09024-5), and the science and technology projects of Shaanxi Province (2009K12-02). We thank Prof. Yonglie Chu of Xi'an Jiaotong University for proofreading, Prof. Yuxin Yin of Columbia University Medical Center for technical assistance and the members of the Department of Oncology, First Hospital of Xi'an Jiaotong University for advice and suggestions.
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Kong, Y., Bai, Ps., Sun, H. et al. Expression of the Newly Identified Gene CAC1 in the Hippocampus of Alzheimer’s Disease Patients. J Mol Neurosci 47, 207–218 (2012). https://doi.org/10.1007/s12031-012-9717-5
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DOI: https://doi.org/10.1007/s12031-012-9717-5