Topic: microglial phagocytosis

Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) and tau neuropathology, neuroinflammation, lipid dysregulation, and progressive loss of cognitive functioning. We have evidence that early dietary interventions with ω6/ω3 polyunsaturated fatty acids (PUFAs) can protect against cognitive decline and lastingly alter microglia and brain lipid profile in the context of early-life stress​. PUFAs can directly modulate microglia. In the context of AD, it is unknown if lipid and PUFA derivatives (oxylipins) are dysregulated in the brain, how these rel

Alzheimer's Disease (AD) are characterized with the accumulation of hyperphosphorylated tau protein and Aβ and neuroinflammation. Disrupted myelin has been observed in the brains of AD patients before the onset of symptoms. However, it remains unknown the function of myelin-forming cells in AD pathogenesis. Oligodendrocyte precursor cells (OPCs) are the source cells of myelin-forming cells in the central nervous system (CNS). In this study, we observe an abnormally enhanced microglial phagocytosis upon in activation of autophagy in OPCs. AD transgenic mice harboring defective autophagy exhibit