With the acceleration of the aging trend, the incidence of Alzheimer's disease (AD) has increased year by year. The disease is a central nervous system disorder characterized by cognitive dysfunction and memory impairment. Abnormal mitochondrial structure and function is one of the pathogenesis factors of AD, and nicotinamide mononucleotide
promotes mitochondrial energy metabolism, which plays an important role in improving cognitive function and memory function. The CAS number of nicotinamide mononucleotide is 1094-61-7. The study found that when the level of NMN
in the body is increased, the availability of NAD+ is increased, the mitochondrial oxygen consumption rate (OCR) is increased, the mitochondrial fusion is promoted, the fission tendency is reduced, and the mitochondria produce longer mitochondria in the hippocampus region, thereby improving mitochondrial respiratory function. The β-amyloid β-protein (Aβ) is considered to be the main neurotoxic agent leading to AD. The study found that NMN improved the cognitive and memory functions of Alzheimer's disease rats induced by Aβ1-42 oligomers, restored the levels of NAD+ and ATP, and reduced the accumulation of ROS (reactive oxygen species) in hippocampal slices of AD mice by improving energy metabolism and inhibiting oxidative s By activating c-Jun N-terminal kinase (JNK), NMN improves behavioral cognitive impairment in AD mice, inhibits β-amyloid production, and reduces amyloid plaque burden, synaptic damage and inflammatory responses in the nervous system. The above experiments show that NMN can be used as a potential drug for the treatment of AD.