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Microglial activation as a hallmark of neuroinflammation in Alzheimer’s disease
Activation of brain immune cells as a key sign of inflammation in Alzheimer's disease
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Abstract
Microglial activation is a key feature of neuroinflammation in Alzheimer's disease (AD).
- The formation and accumulation of amyloid beta (Aβ) peptide and neurofibrillary tangles contribute to synaptic dysfunction and neuronal death.
- Aβ oligomers may trigger microglial activation, leading to increased release of pro-inflammatory cytokines.
- Activated microglia surrounding amyloid plaques are associated with heightened production of cytokines such as interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α).
- Chronic microglial activation could lead to enhanced tau pathology and neuronal apoptosis.
- Microglial activation exhibits dual characteristics, including both inflammatory (M1) and anti-inflammatory (M2) phenotypes, influenced by the microenvironment.
- Disruption in microglial function may contribute to neurovascular dysfunction and cognitive decline in AD.
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