NMN activates Sirtuins to counteract brain aging

NMN demonstrates significant biological potential in offsetting brain aging by activating the Sirtuins protein family, especially SIRT1 and SIRT3. The mechanism involves multi-dimensional synergistic effects such as energy metabolism regulation, oxidative stress relief, neuroprotection, and gene expression regulation.

association between Sirtuins and brain aging

Sirtuins are a class of NAD⁺ -dependent deacetylases, including seven members from SIRT1 to SIRT7, which are widely distributed in brain neurons, glial cells and vascular endothelial cells.

With the increase of age, the decline in NAD⁺ levels leads to a decrease in Sirtuins activity, which in turn causes age-related pathological changes such as mitochondrial dysfunction, increased oxidative stress, release of inflammatory factors and neuronal apoptosis.

For instance, SIRT1 plays a crucial role in regulating neuronal survival, synaptic plasticity and synaptic formation. The decline in its activity is closely related to the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD).

mechanism by which NMN activates Sirtuins

As a precursor of NAD⁺, NMN directly activates Sirtuins family proteins by supplementing the level of NAD⁺ within cells.

Sirt1-dependent neuroprotection

Activation of SIRT1 can inhibit the expression of pro-apoptotic genes such as p53 and FoxO3a, and reduce neuronal apoptosis.

Promote the secretion of brain-derived neurotrophic factor (BDNF), enhance synaptic plasticity and learning and memory abilities;

Regulate the NF-κB signaling pathway, inhibit the activation of microglia and neuroinflammation.

Sirt3-mediated mitochondrial homeostasis

SIRT3 activates the mitochondrial respiratory chain complex through deacetylation, enhancing the efficiency of ATP production.

Inhibit the opening of mitochondrial permeability transition pores (mPTP), reduce the release of cytochrome C and the apoptotic signal cascade;

Regulate the activity of antioxidant enzymes (such as SOD2), reduce the level of reactive oxygen species (ROS), and alleviate oxidative damage.

Relevant research

The research of the School of Medicine, Zhejiang University in 2022

The research team's published results show that after supplementing NMN, the expression of SIRT2 was activated and the myelin regeneration ability was restored, demonstrating the great potential of NMN in preventing the aging of the nervous system.

As people age, a significant manifestation of brain decline is myelin aging, which in turn drives the aging of the central nervous system (CNS), thereby triggering neurodegenerative diseases.

Supplementing NMN can increase the level of NAD+, induce SIRT2 to enter the cell nucleus, restore the vitality of oligodendrocyte progenitor cells, ultimately delay the myelin aging of the normal central nervous system, and enhance the myelin regeneration ability of the central nervous system.

Tag: NMN

Supplier Introduction: China glutathione supplier and NMN manufacturer GSHworld, the company mainly develops biotechnology and industrialization. As a global pioneer in enzymatic catalytic ATP regeneration technology, our company advocates green production and is committed to providing customers with better and more environmentally friendly products and services. Glutathione Manufacturer,NMN Factory,Citicoline Sodium supplier,China NMN manufacturers