Aberrant energy metabolism in Alzheimer’s disease

Author:

Yu Linjie1234,Jin Jiali1234,Xu Yun1234,Zhu Xiaolei1234

Affiliation:

1. Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Drum Tower Hospital, Nanjing University , Nanjing 210008 , Jiangsu Province , China

2. Institute of Brain Sciences, Nanjing University , Nanjing 210008 , Jiangsu Province , China

3. Jiangsu Key Laboratory for Molecular Medicine, Medical School of Nanjing University , Nanjing 210008 , Jiangsu Province , China

4. Nanjing Neuropsychiatry Clinic Medical Center , Nanjing 210008 , Jiangsu Province , China

Abstract

Abstract To maintain energy supply to the brain, a direct energy source called adenosine triphosphate (ATP) is produced by oxidative phosphorylation and aerobic glycolysis of glucose in the mitochondria and cytoplasm. Brain glucose metabolism is reduced in many neurodegenerative diseases, including Alzheimer’s disease (AD), where it appears presymptomatically in a progressive and region-specific manner. Following dysregulation of energy metabolism in AD, many cellular repair/regenerative processes are activated to conserve the energy required for cell viability. Glucose metabolism plays an important role in the pathology of AD and is closely associated with the tricarboxylic acid cycle, type 2 diabetes mellitus, and insulin resistance. The glucose intake in neurons is from endothelial cells, astrocytes, and microglia. Damage to neurocentric glucose also damages the energy transport systems in AD. Gut microbiota is necessary to modulate bidirectional communication between the gastrointestinal tract and brain. Gut microbiota may influence the process of AD by regulating the immune system and maintaining the integrity of the intestinal barrier. Furthermore, some therapeutic strategies have shown promising therapeutic effects in the treatment of AD at different stages, including the use of antidiabetic drugs, rescuing mitochondrial dysfunction, and epigenetic and dietary intervention. This review discusses the underlying mechanisms of alterations in energy metabolism in AD and provides potential therapeutic strategies in the treatment of AD.

Publisher

Walter de Gruyter GmbH

Subject

Internal Medicine

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