As people age, under the influence of chronic stress or neurodegenerative diseases, the brain is prone to problems such as a decline in NAD⁺ levels, mitochondrial dysfunction, and intensified neuroinflammation, which in turn can trigger memory loss, cognitive impairment, and even diseases like Alzheimer's and Parkinson's.
NMN can provide multi-dimensional protection for brain health by increasing the level of NAD⁺ in brain nerve cells and activating neuroprotective and metabolic regulatory pathways.
Optimize energy metabolism of nerve cells and maintain efficient operation of brain
Nerve cells (especially neurons) have an extremely high demand for energy - the brain accounts for only 2% of a person's body weight but consumes 20% of the body's energy, and this energy mainly depends on the synthesis of ATP in the mitochondria of neurons.
Under conditions of aging or neurodegenerative diseases, the level of NAD⁺ in brain nerve cells significantly decreases, which inhibits the activity of the mitochondrial respiratory chain, leading to insufficient ATP production. This, in turn, affects the electrical signal transmission and neurotransmitter synthesis of neurons, causing problems such as inattention and slow thinking.
The optimization of energy metabolism in nerve cells by NMN is reflected in two aspects:
On the one hand, supplementing NMN can rapidly increase the level of NAD⁺ within neurons. NAD⁺ is a key coenzyme in the mitochondrial respiratory chain (complexes I, II, and III), which can promote the oxidative decomposition of glucose and fatty acids and accelerate ATP synthesis.
On the other hand, SIRT3 (mitochondrial deacetylase) activated by NMN can regulate the activity of metabolic enzymes in the mitochondrial matrix (such as citrate synthase and succinate dehydrogenase), repair damaged mitochondrial structures, enhance the efficiency of mitochondrial oxidative phosphorylation, and provide continuous and stable energy supply for nerve cells.
Protect integrity of nerve cells and reduce neurodegenerative damage
The integrity of nerve cells is the foundation of brain function, and oxidative stress and toxic protein deposition (such as β -amyloid protein in Alzheimer's disease and α -synuclein in Parkinson's disease) are the main triggers leading to nerve cell apoptosis.
Research has found that a decline in NAD⁺ levels weakens the antioxidant capacity and toxic protein clearance ability of nerve cells, accelerating neuronal death and the formation of neurofibrillary tangles.
NMN protects nerve cells through three mechanisms:
Firstly, after NMN increases the level of NAD⁺, it can activate SIRT1 (Silent Information Regulator 1). SIRT1 can enhance the activities of superoxide dismutase (SOD) and Glutathione peroxidase (GSH-Px) within nerve cells, eliminate excessive reactive oxygen species (ROS), and alleviate oxidative stress damage.
Secondly, NMN can activate the autophagy pathway (mTOR signaling regulated by NAD⁺), promoting the degradation and clearance of toxic proteins within neurons and reducing the toxic effects of protein deposition on nerve cells.
Thirdly, NMN can maintain the stability of nerve cell membranes by enhancing the activity of NAD⁺ -dependent PARP1 (DNA repair enzyme), repairing DNA damage in nerve cells caused by oxidative stress, and reducing the apoptosis rate of neurons.
Promote synthesis of neurotransmitters and improve emotional and cognitive functions
Neurotransmitters are the "chemical messengers" that transmit signals between nerve cells, such as acetylcholine (regulating learning and memory), dopamine (regulating mood and motivation), serotonin (regulating mood and sleep), etc. Their synthesis and metabolism rely on NAD⁺ as a coenzyme.
When the level of NAD⁺ in the brain drops, the activity of neurotransmitter synthases (such as choline acetyltransferase and tyrosine hydroxylase) decreases, which can lead to an imbalance of neurotransmitters and cause problems such as memory loss, depression and anxiety.
NMN regulates the balance of neurotransmitters through two pathways:
On the one hand, supplementing NMN can increase the level of NAD⁺ in the brain, providing sufficient coenzymes for neurotransmitter synthase and promoting the synthesis of neurotransmitters such as acetylcholine and dopamine. For instance, NAD⁺ is an essential coenzyme for tyrosine hydroxylase (a key enzyme in dopamine synthesis), and an increase in NAD⁺ levels can enhance the activity of this enzyme by 35%, directly increasing dopamine production.
On the other hand, NMN-activated SIRT1 can regulate the expression of neurotransmitter transporters (such as serotonin transporter SERT), reduce the recycling of neurotransmitters in the synaptic cleft, prolong the action time of neurotransmitters, and enhance the efficiency of neural signal transmission.
Inhibit chronic inflammation of brain and alleviate neuroinflammatory damage
Chronic neuroinflammation is an important driver of age-related cognitive decline and neurodegenerative diseases. When the brain is infected, injured or exposed to toxic stimuli, microglia (immune cells in the brain) are overly activated, releasing a large amount of inflammatory factors (such as TNF-α, IL-6, IL-1β). These inflammatory factors can damage neuronal synapses and disrupt neural connections, which may lead to a decline in cognitive function in the long term.
Studies have shown that a decline in NAD⁺ levels can enhance the inflammatory response of microglia and exacerbate neuroinflammation.
NMN inhibits chronic inflammation in the brain through dual mechanisms:
Firstly, after NMN increases the level of NAD⁺, SIRT1 can directly deacetylate the inflammatory transcription factor NF-κB (nuclear factor κB), preventing it from entering the cell nucleus and initiating the expression of inflammatory factor genes, thereby reducing the release of inflammatory factors by microglia from the source.
Secondly, NMN can improve the mitochondrial function of microglia and reduce the generation of mitochondrial reactive oxygen species (mtROS) - mtROS are key "signaling molecules" that activate the inflammatory response of microglia. Reducing their release can inhibit the excessive activation of microglia and alleviate the damage of inflammation to neurons.
Protect function of cerebral blood vessels and maintain blood supply to brain
The cerebral blood vessels are the "channels" for the brain to obtain oxygen and nutrients. Abnormal functions of cerebral endothelial cells (such as decreased vasodilation ability and damaged blood-brain barrier) can lead to insufficient blood perfusion to the brain, causing cerebral hypoxia and nutrient supply disorders, which in turn affect the function of nerve cells.
As people age, the level of NAD⁺ in cerebral vascular endothelial cells decreases, which leads to a reduction in the production of nitric oxide (NO, a key molecule regulating vasodilation), a decrease in vascular elasticity, and an increased risk of cerebral infarction and cognitive impairment.
NMN protects cerebrovascular function through two pathways:
On the one hand, NMN increases the level of NAD⁺ in cerebral vascular endothelial cells, activates SIRT1, promotes the deacetylation of endothelial nitric oxide synthase (eNOS), enhances eNOS activity, and increases NO production - NO can relax the smooth muscle of cerebral blood vessels, dilate blood vessels, and increase cerebral blood perfusion.
On the other hand, NMN can enhance the integrity of the blood-brain barrier by increasing the expression of NAD⁺ -dependent tight junction proteins (such as occludin and claudin-5), reducing the entry of harmful substances into the brain through the blood-brain barrier, and at the same time preventing the loss of nutrients in the brain.
