Myricetin Restores Aβ-Induced Mitochondrial Impairments in N2a-SW Cells

Alzheimer's disease (AD) is the most common type of dementia that occurs in the elderly. Amyloid hypothesis is one of the most studied pathological mechanisms, and fi-amyloid (Afi) is the drug target for most clinical trials. Mitochondrial dysfunction induced by the Afi-precursor protein (APP)/Afi has been suggested to play a key role in the development of AD. Here, we explored the effects of myricetin, a polyphenol compound abundant in fruits and vegetables, on mitochondrial damages in N2aSW cells. After the treatment of myricetin, mitochondrial depolarization was improved by increasing the mitochondrial membrane potential. Mitochondrial biogenesis as well as mitochondrial genome integrity was enhanced via increased levels of PGC-1a, Nrf1, TFAM, and the copy number of mtDNA. Mitochondrial functions were restored as represented by the increased levels of proteins involved in the electron transport chain and the adenosine 5 '-triphosphate (ATP) content and the decreased concentration of ROS. Mitochondrial dynamics and mitophagy were ameliorated through the regulation of proteins involved in fusion (OPA1 and Mfn2), fission (Drp1 and Fis1), and mitophagy (PINK1 and Parkin). Thus, it is summarized that myricetin could recover the mitochondrial impairments in N2a-SW cells, exhibiting the potential to promote neuroprotection for APP/Afi-related diseases, including AD.

Automated summary

This study explored the effects of myricetin, a polyphenol compound abundant in fruits and vegetables, on mitochondrial damages in N2a-SW cells. The results showed that myricetin improved mitochondrial depolarization and increased mitochondrial membrane potential, leading to enhanced mitochondrial biogenesis and genome integrity. Additionally, myricetin restored mitochondrial functions, regulated mitochondrial dynamics and mitophagy, suggesting its potential for promoting neuroprotection in APP/Aβ-related diseases, including Alzheimer's disease.