Affiliations: [a] Chongqing Key Laboratory of Neurodegenerative Diseases, Chongqing, Chongqing, China
| [b] Department of Neurology, Chongqing General Hospital, University of Chinese Academy of Sciences, Chongqing, Chongqing, China
| [c] Department of Neurology, Affiliated Hospital of Guangdong Medical University, Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Zhanjiang, Guangdong, China
| [d]
Chongqing Institute of Green and Intelligent Technology, Chinese Academy of Sciences, Chongqing, China
Correspondence:
[*]
Correspondence to: Zhiyou Cai, Department of Neurology, Chongqing General Hospital, University of Chinese Academy of Sciences, No. 312 Zhongshan First Road, Yuzhong District, Chongqing 400013, People’s Republic of China. Tel./Fax: +86 23 63515796; E-mail: caizhiyou@ucas.ac.cn.; Zhou Liu, Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, No. 57 South Renmin Avenue, Xiashan, 524023 Zhanjiang, Guangdong, China. E-mail: liuzhou@gdmu.edu.cn.
Note: [1] These authors contributed equally to this work.
Abstract: Mitochondrial dysfunction has been widely reported in several neurodegenerative disorders, including in the brains of patients with Alzheimer’s disease (AD), Parkinson’s disease, and Huntington disease. An increasing number of studies have implicated altered glucose and energy metabolism in patients with AD. There is compelling evidence of abnormalities in some of the key mitochondrial enzymes involved in glucose metabolism, including the pyruvate dehydrogenase and α-ketoglutarate dehydrogenase complexes, which play a great significance role in the pathogenesis of AD. Changes in some of the enzyme activities of the mitochondria found in AD have been linked with the pathology of amyloid-β (Aβ). This review highlights the role of mitochondrial function in the production and clearance of Aβ and how the pathology of Aβ leads to a decrease in energy metabolism by affecting mitochondrial function.
