Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment, cognitive decline, and behavioral disturbances. There is no effective and safe medication for AD at present. Nicotinamide adenine dinucleotide (NAD+) is a nicotinamide coenzyme regulating metabolic processes such as glycolysis and fatty acid oxidation. NAD+ also acts as a cofactor for several enzymes, including the deacetylases Sirtuins and poly ADP ribose polymerases (PARPs), which are involved in mitochondrial quality control, inflammation, epigenetic DNA regulation, and DNA damage repair. This chapter elucidates the pathological mechanisms of AD related to NAD+ functions, including mitochondrial dysfunction and neuroinflammation. Exogenous supplementation of NAD+ and its precursors can enhance mitochondrial function in cellular and animal models of AD, inhibit neuroinflammation, and improve cognitive abilities as well as learning and memory in AD model animals.

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Nicotinamide Adenine Dinucleotide and Alzheimer’s Disease

  • Ying Cheng,
  • Da-Chuang Yang,
  • Fang Lin

摘要

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment, cognitive decline, and behavioral disturbances. There is no effective and safe medication for AD at present. Nicotinamide adenine dinucleotide (NAD+) is a nicotinamide coenzyme regulating metabolic processes such as glycolysis and fatty acid oxidation. NAD+ also acts as a cofactor for several enzymes, including the deacetylases Sirtuins and poly ADP ribose polymerases (PARPs), which are involved in mitochondrial quality control, inflammation, epigenetic DNA regulation, and DNA damage repair. This chapter elucidates the pathological mechanisms of AD related to NAD+ functions, including mitochondrial dysfunction and neuroinflammation. Exogenous supplementation of NAD+ and its precursors can enhance mitochondrial function in cellular and animal models of AD, inhibit neuroinflammation, and improve cognitive abilities as well as learning and memory in AD model animals.