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Programmed Death of Microglia in Alzheimer's Disease: Autophagy, Ferroptosis, and Pyroptosis

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SPRINGER BASEL AG
DOI: 10.14283/jpad.2023.3

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Alzheimer's disease; cell death; microglia; autophagy; ferroptosis; pyroptosis

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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline, amyloid-beta plaques, and neurofibrillary tangles. Evidence suggests that cell death, including necroptosis, pyroptosis, autophagy, and ferroptosis, plays a crucial role in AD progression. This review focuses on the mechanisms of programmed microglial death, such as pyroptosis, autophagy, and ferroptosis, and their connection to AD.
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, amyloid-beta (A beta) plaques and the formation of neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau. Increasing evidence has demonstrated that the damage of cell plays an important role in AD. Cell death is a critical phenomenon for physiological functions, which promotes AD pathogenesis. Programmed cell death, including necroptosis, pyroptosis, autophagy, and ferroptosis, have been discovered that have unique biological functions and pathophysiological characteristics. Here, we review the available evidence detailing the mechanisms of programmed microglial death, including pyroptosis, autophagy, and ferroptosis. We also highlight the role of programmed death of microglia during the process of AD and focus on the connection between the disease and cell death.

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