The decline in cognitive function associated with aging is thought to be linked to increased oxidative stress, insufficient nutritional support, accumulation of protein aggregates, dysfunction in the neurovascular system, and abnormal activation of the immune system.
Due to the unique structure of the blood-brain barrier, numerous potential components are unable to traverse it and enter the brain. Consequently, substances possessing multiple biological activities and the capability to pass through the blood-brain barrier via small molecules become exceptionally valuable. Fisetin (also known as quercetin) is one such potential component。
Fisetin, also known as quercetin, is a flavonoid component found in strawberries (160 μg/g) and other fruits and vegetables.
It not only exhibits direct antioxidant activity but also increases the levels of the primary antioxidant glutathione within cells. In the presence of oxidative stress, fisetin is capable of maintaining mitochondrial function, protecting neuronal cells from death caused by oxidative stress.
The broad range of these actions suggests that fisetin has the potential to reduce age-related decline in brain function.
Similar to other organs, the functionality of the brain undergoes aging with the passage of time.
A key mechanism contributing to aging is cellular senescence, during which DNA damage, mitochondrial dysfunction, or the accumulation of other cellular stress factors lead cells into a state of replicative arrest and resistance to apoptosis, forming what is commonly referred to as "zombie" cells.
In younger individuals, senescent cells are relatively rare, but with the advancement of age, these cells increase in various tissues. Accumulated "zombie" cells from aging harbor substantial damage and do not undergo apoptosis. Instead, they persistently induce local and systemic chronic inflammation, as well as tissue damage.
Animal studies indicate that transplanting senescent cells into young mice can trigger a series of age-related diseases, whereas removing senescent cells from older mice can improve the health of multiple organ systems and extend lifespan. This highlights the detrimental impact of senescent cells on the aging process and suggests that mitigating their effects may contribute to enhanced overall health and longevity.
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Fisetin has the ability to block the mTOR (mammalian target of rapamycin) signaling pathway, thereby activating autophagy in senescent "zombie" cells and assisting the body in clearing these aging cells.
Based on current research, fisetin can modulate or disrupt various cellular pathways at the molecular level.
For instance, it can inhibit NF-κB (Nuclear Factor Kappa-light-chain-enhance of Activated B Cells), a transcription factor that signals genes to produce inflammatory compounds.
Moreover, studies also suggest that fisetin may enhance long-term memory, indicating its potential utility in treating individuals with memory disorders.
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