Not many years ago, a diagnosis of dementia left little in the line of treatment options. Most times, people watched the progression of cognitive and functional decline in their loved ones. Then the advent of cholinesterase inhibitors provided some relief, albeit not a cure. At least in some people, these drugs could slow the progression of decline. Suppose there is a way to halt the advancement of Alzheimer’s and perhaps even reverse cognitive decline. Imagine the impact this could have on those living with Alzheimer’s and other dementias.
NMN (Nicotinamide Mononucleotide) is a precursor for NAD (Nicotinamide Adenine Dinucleotide), vital to sustaining cell life.
NMN and NAD decline as we age, potentially contributing to age-related conditions such as Alzheimer’s and other types of dementia.
Supplementation with NAD+ precursors, such as NMN, shows promise to prolong cell life and potentially reverse some of the causes of Alzheimer’s in mouse models.
Further research is imperative to study the possibility of NMN reversing Alzheimer’s in humans.
Dementia is an umbrella term describing several neurodegenerative disorders causing impairment of cognition and function. Alzheimer's is the most prevalent type of dementia, affecting around 6.5 million Americans. The probable cause of Alzheimer’s results from the abnormal build-up of beta-amyloid and Tau proteins disrupting nerve conduction in the brain. This nerve cell disturbance is linked to impairment in memory, language, and other brain functions.
Although the actual cause is uncertain, lifestyle, environmental factors, and genetics all play a part in the development of the disease. More recently, scientists have made some advancements in dementia research associated with Nicotinamide Mononucleotide (NMN). Could this be a new direction in not only preventing but possibly reversing the process of Alzheimer’s disease?
What are NMN and NAD+?
Nicotinamide Mononucleotide (NMN) is a molecule called a nucleotide that occurs naturally in the body and is an immediate precursor or building block for Nicotinamide Adenine Dinucleotide (NAD). NMN converts to NAD+, a vital co-enzyme found in every cell in the body; without it, cells would die. NAD+ works with specific proteins called sirtuins to help repair DNA and support energy metabolism. Having enough NAD+ to sustain cell life means having an abundance of NMN.
While we are young, our system has sufficient levels of NMN. However, as we age, the levels of NMN significantly decline, decreasing the production of NAD+. The reduction in NAD+ may lead to cellular dysfunction, contributing to age-related issues, such as reduced energy, cognitive decline, and the potential development of chronic illnesses such as diabetes, liver and kidney disease, and cardiovascular illness.
NMN from whole foods added to your diet may increase NMN levels. However, we require more research to validate if eating NMN-rich foods is adequate to increase cellular NAD+ levels.
NMN is readily available in whole foods such as:
|NMN amount per 100 g
NMN has been receiving more attention lately as an anti-aging supplement. As we grow older, DNA damage increases due to environmental influences such as radiation and pollution. Therefore, the research has been trying to address whether increasing the level of NMN has the potential to repair DNA and slow the aging process. However, the US Food and Drug Administration (FDA) has recently declared the prohibition of marketing and selling NMN as a dietary supplement. This ban is due to NMN being investigated as a potential new drug.
Role of NMN in dementia and Alzheimer’s
Studies have emerged researching the potential of NMN in age-related cognitive diseases such as Alzheimer’s (AD) and other types of dementia.
For example, in 2017, one research study carried out at Tongji University in Shanghai showed that NMN supplementation in mice model of Alzheimer's disease was associated with improvement in several aspects of AD pathology. The results indicated that mice with Alzheimer's treated with NMN had reduced beta-amyloid protein production and reduction of inflammation. Scientists also found that the mice treated with NMN displayed improved memory and spatial learning compared to the untreated mice.
In another study, supplementation with NAD+ precursor, namely nicotinamide riboside (NR), was linked to reduced inflammation in neurons, improved cognitive function, and reduced DNA damage in mouse model of Alzheimer's disease. In addition, other critical elements found in Alzheimer’s disease were also affected, including reduced accumulation of the abnormal Tau protein and decreased neuron degeneration.
More recently, research published in March 2022 out of the Shanghai Institute for Chinese Medicine studied the impact on Alzheimer’s disease by boosting levels of NAD+. This study confirmed that by increasing NAD+ precursors in mice with AD, there is a reduction in amyloid plaque and the reduced inflammatory response associated with AD.
While research shows promise regarding the possible benefits of boosting NAD+ with supplementation of its precursors, such as NMN, it has mainly focused on animal models to study its effectiveness. Much more research on humans is needed to progress to the stage of actual treatment for diseases related to aging, such as Alzheimer’s and other types of dementia. The FDA’s move to remove NMN from the classification of a dietary supplement may indicate a step toward pharmaceutical development in the future. The potential to reverse the critical element of Alzheimer’s disease could undoubtedly be a pivotal event in dementia research.
Please be aware that from the fall of 2022 NMN is under an investigation as a potential new drug by the FDA. That puts the legality of the product as a dietary supplement in question. It’s a complicated situation that’s not yet solved. However, it is important to note that since we are not a manufacturer or retailer, we do not take any responsibility for the availability of the product as a dietary supplement after having lost its dietary ingredient status.
- Frontiers in Cell and Developmental Biology. NAD+ in Alzheimer’s Disease: Molecular Mechanisms and Systematic Therapeutic Evidence Obtained in vivo.
- Neuroscience Letters. Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer's disease.
- PNAS. NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency.
- Trends in Molecular Medicine. NAD+ in Aging: Molecular Mechanisms and Translational Implications.
- Biological Research. Aβ promotes CD38 expression in senescent microglia in Alzheimer’s disease.
- Cell Metabolism. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice.