NMN found to improve mitochondrial function in age-related diseases

AD is the most common cause of dementia in the elderly, and aging is the most important risk factor.

Mitochondrial dysfunction is a hallmark of aging and has been found in various age-related diseases. Recent studies in animal models have shown that mitochondrial dysfunction is the main feature of AD, and enhancing mitochondrial function has become a potential treatment for AD. NMN was found to improve mitochondrial function in age-related diseases. Long et al. injected NMN into APP/PS1 mice, observed mitochondrial morphology, measured oxygen consumption, and measured APP, Sirt1, PGC-1α in mice, and found that respiratory function returned to normal, APP decreased, and levels of Sirt1 and PGC-1α increased and normalized mitochondrial morphology, indicating that NMN improves mitochondrial bioenergetics and dynamics; NMN was also found to compensate for the loss of NAD+ in AD mouse models and reduce mitochondrial fragmentation in mice with fluorescent proteins targeting neuronal mitochondria , without any side effects.

Experiments by Chandrasekaran et al also show that NMN treatment can improve diabetes-induced reduction in mitochondrial respiration, prevent diabetes-induced cognitive impairment and reduce the number of hippocampal neurons.

Hosseini et al. administered NMN and melatonin alone or in combination to rats (3 months and 24 months) for 28 days, using Barnes maze and novel object recognition test to evaluate spatial memory and episodic memory, and found that NMN The use of melatonin alone or in combination can delay aging-induced memory impairment; by measuring reactive oxygen species, ATP levels and mitochondrial membrane potential, the apoptosis and mitochondrial function changes in the prefrontal cortex and hippocampus were assessed, and the results showed that Combined administration reduced mitochondrial dysfunction and the number of apoptotic cells in the prefrontal cortex and hippocampus. This experiment suggests that NMN and melatonin alone or in combination (more effectively) may enhance neuroprotection and improve cognitive function by inhibiting mitochondrial permeability and enhancing antioxidant pathways.

However, in the above study, it was administered at a low dose (100 mg/kg), and it is unclear whether a higher dose of NMN or a longer duration of administration will achieve better results.

Aβ oligomers are the main neurotoxic drugs for the treatment of AD. They form amyloid plaques in the brains of AD patients and also inhibit the long-term gain (LTP) effect of the hippocampus. NMN was found to protect cognitive impairment caused by Aβ oligomers. Yao et al. subcutaneously injected NMN into APP/PS1 mice to explore whether NMN could reverse AD by inhibiting the activation of JNK, and found that NMN treatment largely improved the main pathological features of the AD model mice, including cognitive impairment, Neuroinflammation, Aβ pathology, and synaptic damage, experiments show that NMN treatment inhibits APP JNK activation and amyloidogenic processes by mediating the expression of APP cleavage secretase, demonstrating that NMN reverses AD at least in part by inhibiting JNK activation.

Tarantini et al. found that supplementing NMN in aged mice could increase NO-mediated vasodilation in endothelial cells to rescue the NVC (neurovascular coupling) response and improve cognitive function, demonstrating that NMN has a protective effect on brain microvascular in aged mice.

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