Accumulating evidence indicates that mitophagy is also impaired in AD patient, as well as mouse models, and is linked to the development and progression of the disease in several ways. This process is important for maintaining the homeostasis of cells, and the dysregulation of mitophagy has been implicated in the progression of neurodegenerative diseases. Mitophagy is the process by which cells remove and recycle impaired mitochondria. Mitochondria impairment has been shown to occur in early AD patients, potentially contributing to brain cell death and inflammation, which are hallmarks of Alzheimer’s disease. Together, these results supported the important role of mitophagy in AD pathogenesis and suggested that galangin may be used as a novel mitophagy enhancer to treat AD.Īccumulating evidence suggests that mitochondria, the main energy-producing organelles in cells, play a critical role in the development of Alzheimer’s disease (AD). The effect of galangin was blocked by the mitophagy inhibitor, suggesting that galangin possibly acted as a mitophagy enhancer to ameliorate Aβ-induced pathology. Notably, galangin (10 μM) treatment restored mitophagy and organoid growth, which was inhibited by Aβ. Further analysis revealed that mitophagy levels were reduced in the brain organoids and NPCs. Moreover, Aβ treatment inhibited neural progenitor cell (NPC) growth and induced mitochondrial dysfunction. Here, by using a novel 3D human brain organoid culturing system, we found that amyloid-β (Aβ 1-42,10 μM) decreased the growth level of organoids, indicating that the neurogenesis of organoids may be impaired. It is imperative to create appropriate preclinical models to study the role of mitophagy in AD and to assess potential mitophagy-targeting therapies. ![]() It is widely accepted that restoration of mitophagy helps to maintain cellular homeostasis and ameliorates the pathogenesis of AD. Dysfunctional mitochondria and mitophagy are hallmarks of Alzheimer’s disease (AD).
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