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An estimated 5.7 million Americans lived with Alzheimer’s disease in 2018, according to the Centers for Disease Control (CDC). Alzheimer’s disease can seriously affect one’s ability to perform daily activities and involves a deterioration in parts of the brain controlling thought, memory, and language.

Although scientists don’t know the exact cause of the disease, they believe a combination of genetic, lifestyle, and environmental factors contribute to the onset of Alzheimer’s disease. The results of disease onset include disruption of brain cell function, with damaged brain cells that have lost connections and often die. In the brain, abnormal protein disrupts normal brain functions, such as  the plaque forming toxic ß-amyloid accumulation and protein tangles called neurofibrillary tangles. Ongoing studies continue with the hope of uncovering a better understanding of the cause as well as treatment options.

In 2017, a team of scientists from Tongji University in Shanghai and Nanjing Medical University in Nanjing found nicotinamide mononucleotide (NMN) reversed the effect of Alzheimer’s disease in mice. NMN boosted levels of nicotinamide adenine dinucleotide (NAD+) in cells, which researchers have associated with improvements in age-related diseases in animal models. The molecule not only improved the cognitive function in diseased mice, but also decreased the production of toxic protein in the brain and reduced the inflammatory response caused by Alzheimer’s disease.

The group of scientists found significantly improved spatial learning, an indicator of cognitive function, in mice with Alzheimer’s disease treated with NMN. While mice with Alzheimer’s disease had a reduced performance in a spatial learning task, diseased-mice treated with NMN improved their cognitive performance and performed almost as well as normal mice.

(Yao et al., 2017 | Neuroscience letters) Mice with Alzheimer’s disease perform better on a task measuring cognition following NMN. WT denotes normal mice and Tg means mice with Alzheimer’s disease. The bar on the far-right side shows mice with Alzheimer’s disease administered NMN performing almost as well as normal mice.


NMN treatment also lowered the level of amyloid ß oligomers, a toxic protein that forms plaques that build up in the brains of Alzheimer’s patients. When the researchers looked at the plaque build-up in the brain under a microscope, they found the amount of plaques in mice with Alzheimer’s disease dropped after NMN treatment. .

(Yao et al., 2017 | Neuroscience letters) NMN reduces the plaque build up in the brains of mice with Alzheimer’s disease. The image on the left shows the brown plaque build ups in mice with Alzheimer’s disease. The image on the right shows the reduction in brown plaque build up following NMN treatment in mice with Alzheimer’s disease.


NMN treatment improved neural inflammation in mice with Alzheimer’s disease. Levels of molecules associated with neural inflammation were presented at lower levels in mice with Alzheimer’s disease treated with NMN compared to those not treated with NMN.

“According to our findings, NMN could be a new target for disease-modifying treatments in [Alzheimer’s disease],” stated the authors in their study. With substantially improving cognitive function, lowering amyloid plaque build up, and improving neuroinflammation in mice, NMN could provide a valuable therapeutic option for Alzheimer’s disease in the future.