Cognitive decline is an unfortunate part of the aging process.
As we grow older, our risk of Alzheimer’s disease (AD) increases. The neurodegenerative disorder impacts the brain’s cognitive and memory functions – and current treatment options are limited. Today AD is estimated to affect 44 million people worldwide.
While there is no known cure for AD, supplementation may be able to slow or prevent the progression of the disease. Studies conducted on the effects of nicotinamide mononucleotide (NMN) supplementation in mice and rats, for example, reveal significant treatment potential.
In this post, we will examine the potential of NMN as a treatment for cognitive decline and age-related diseases like AD. We will discuss what NMN is, examine how it works and explore the limitations of the current research on how it might improve symptoms of AD.
AD is a progressive brain disorder resulting in neuronal damage and impaired cognitive function. The disease is the most common cause of dementia – affecting patients’ memory, mood and behavior.
Alzheimer’s disease generally begins slowly and gets worse over time. Gradually, it may disrupt a person’s daily life. Early symptoms of AD include:
- Difficulty performing tasks
As symptoms progress, AD patients may also experience:
- Mood and behavioral changes
- Language problems
- Impaired judgment
While there is no cure for AD, certain medications, supplements and other treatments can help patients manage their symptoms. Research is ongoing – and studies indicate that NMN supplementation may play a role in preventing neuronal damage and slowing the progression of AD.
What Is NMN?
A reminder that as a person ages, they become more susceptible to neuronal damage and cognitive decline.
NMN may be able to help counteract this. Studies show that the naturally-occurring molecule has neuroprotective effects.
Produced by the body, NMN is a precursor to nicotinamide adenine dinucleotide (NAD+): a coenzyme that plays an important role in DNA repair, energy metabolism and cellular signaling.
NAD+ is found in all of the body’s cells. Without it, the cells wouldn’t be able to survive.
This isn’t an issue in young people. Early in life, we have all of the NAD+ we need. Yet over time, the level of NAD+ in the body declines significantly. This leads to cellular damage, energy deficiencies and other health conditions. Experts have found that a lack of NAD+ not only contributes to age-related decline, but to the onset of health conditions like AD.
This is where supplementation may come in. By supplementing with NMN, researchers believe the body can increase its production of NAD+ and ultimately slow the aging process.
NMN as a Potential Treatment for AD
NMN supplementation has been found to prevent cognitive decline in aged mice and rats with AD. While the research is somewhat limited, the results may well translate to human beings.
Existing animal studies show great promise. For example, a recent study published in Innovations in Aging explored the effects of NMN supplementation on cognitive function in older mice (1). The study focused on 24-month-old mice (the equivalent of 70-year-old human beings) with AD. The mice were treated with NMN over two weeks.
The researchers found that adjusting cerebral blood flow (CBF) via neurovascular coupling (NVC) – a critical mechanism that supplies the brain with energy substrates from the blood – could help maintain healthy brain function in the mice.
Impaired NVC, conversely, leads to cognitive decline. And there is evidence that a decrease in NAD+ over time can exacerbate the problem. In fact, researchers saw that the aged mice’s NVC responses were impaired – yet they found that NMN supplementation could restore their NVC responses.
The study ultimately determined that a decrease in NAD+ supply contributed to age-related cerebral dysfunction in the mice, which magnified their cognitive decline (1). With NMN supplementation, however, the mice improved their coordination and spatial working memory. In other words, they began to overcome some of their AD symptoms.
This reinforces NMN as a potential AD treatment or neuroprotective solution for human beings as well.
More Evidence that NMN Can Improve Cognition
Another study published in Brain Research conducted similar research – this time on rats with AD (2). The researchers found that NMN supplementation could restore cognitive function and decrease amyloid beta (Aβ) accumulation in the cognitively-impaired rats.
Aβ, it’s worth noting, is a protein that accumulates in the brain. Aβ toxicity is linked to AD – and the study found that NMN supplementation reduced Aβ buildup. It also helped to improve neuron survival, increase energy metabolism and reduce the accumulation of reactive oxygen species (ROS).
ROS is an unstable molecule that plays a role in cognitive impairment. The increased levels of NAD+ in the rats’ brains promoted healthy cognition by activating a protein called SIRT1 and producing anti-oxidative enzymes.
The outcome was reduced neuronal damage and increased cognitive function in the rats (2). The results suggest that NMN supplementation can help rats with AD prevent cognitive damage and restore their neuronal health. This shows that NMN supplementation may serve as an equivalent treatment option for human patients with AD and other neurodegenerative diseases.
NMN supplementation has been found to offer neuroprotective effects in older mice and rats with AD. The cognitive-enriching effects of NMN supplementation are the result of activated SIRT1 and the promotion of anti-oxidative pathways. These benefits will likely translate from animal models to human ones – helping people prevent neuronal damage as they age.
In recent years, NMN supplementation has been in the spotlight as a way to prevent or slow the aging process. While more research is needed on human beings, the molecule offers great promise. NMN can also improve eyesight, mitigate hearing loss and enhance overall physiological health.
1. Tarantini, Stefano et al. “NMN rescues endothelial function and neurovascular coupling, improving cognitive function in aged mice.” Innovation in Aging vol. 4, supp. 1 (2020): 121. doi.org/10.1093/geroni/igaa057.399.
2. Wang, Xiaonan et al. “Nicotinamide mononucleotide protects against β-amyloid oligomer-induced cognitive impairment and neuronal death.” Brain research vol. 1643 (2016): 1-9. doi:10.1016/j.brainres.2016.04.060