Both human and mouse data suggests that nicotinamide mononucleotide (NMN) could help to slow the progression of Alzheimer’s disease (AD) by targeting mitochondria. Mitochondria are like our powerhouses; they are a form of energy that our cells utilize to keep us alive. Ounce per ounce, the brain has the highest demand for this energy making the mitochondria paramount in keeping brain cells alive.
In patients with AD their mitochondrial stress is heightened, suggesting damage to the tiny powerhouses, making the mitochondria play fundamental roles in the etiology of diseases caused by brain cell death and damage (neurodegeneration) such as Alzheimer’s disease.. Additionally in mice models of the brain wasting disease, NMN has been found to help alleviate memory loss and neurodegeneration which is the primary symptom and disease pathology in humans.
Recently a study published in Cell Death & Disease highlighted the central importance of the mitochondria in Alzheimer’s disease, suggesting that the NAD+ precursor NMN can target the generally accepted underlying basis of the disease to prevent neurodegeneration.
Investigating mitochondrial stress in Alzheimer’s disease
To come to their conclusion, blood samples from patients with Alzheimer’s disease were analyzed which revealed high levels of circulating mitochondrial stress response proteins (MRS) which are stimulated by various cellular dysfunctions such as mitochondrial damage and oxidative stress that are hallmarks of aging. MRS also includes mitophagy which is a recycling process cells use to remove damaged mitochondria.
Further investigation revealed that the level of MRS proteins circulating in the blood of AD patients could accurately predict diagnosis of the disease, suggesting that AS is associated with MRS in humans. While further investigation is required, the elevated MRS levels could be a sign of conflict between the MRS and various cellular dysfunctions that initiate MRS. Meaning that in Alzheimer diseases brain cells attempts by MRS to alleviate mitochondrial damage and oxidative stress may be ongoing or failing.
NMN Slows progression of AD
Additional investigation involved mice models of Alzheimer’s disease that were injected with 500 mg/kg/day of NMN for two months to study the effects of the NAD+ precursor. The animals also underwent a series of cognitive tests which revealed that the treatments counteracted memory loss and that the memory improvements were mediated by one of the MRS proteins called ATF4, suggesting that NMN slow progression by improving MRS efficiency.
According to the researchers, signs of NMN counteracting the disruption of synapse communication were also found, and NMN was shown to prevent brain atrophy as well as stimulating cellular energy production. When taken together, this suggests that NMN helps to improve memory and halt neurodegeneration in transgenic AD mouse models by targeting MRS.
More research required
Although elevated levels of MRS were found circulating in the blood of AD patients, additional research is required to determine how this is affected by NMN supplementation. Previous research has shown the other NAD+ precursors such as nicotinamide riboside (NR) could slow progression of the disease; it was accompanied by other compounds as part of a cocktail.
Future studies may show that NAD+ precursor to play a preventative role in Alzheimer’s disease which could possibly be related to byproducts of modern civilization such as microplastics that trigger mitochondrial damage and oxidative stress. But further research needed to determine if this is the case or some other cause.
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References/Sources/Materials provided by:
https://www.nature.com/articles/s41419-024-07062-1
https://www.madrc.org/wp-content/uploads/2023/12/NMN-AD-Study-Flyer-20231116.pdf
https://www.brighamandwomens.org
https://www.nad.com/news/hallmarks-of-aging-reversed-therapy
