Microglia in Alzheimer's Disease
By Ying Li, M. Tan, Teng Jiang, L. Tan. BioMed Research International, 2014
784 citations recorded by the source corpus.
Alzheimer's disease (AD) is a familiar neurodegenerative disease in the elderly. In this paper, we will review current viewpoints of microglial activation, inflammatory regulatory systems, and their relationship with AD pathology and etiology. Microglia cells are macrophage and representative of the innate immune system in brain. AD brain is marked by obvious inflammatory features, in which microglial activation is the driving force. β-amyloid protein sedimentation activates microglia cells, which causes the inflammation in AD. Microglia cells have dual roles: they provoke the release of inflammatory factors and cytotoxins leading to neuronal injuries and death; on the other hand, they have the neuroprotective effects. Through this, we hope to illustrate that the anti-inflammatory defenses of neurons can be practiced in the future strategy for recuperating the balance between the levels of inflammatory mediators and immune regulators in AD.
Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/9d757a0ef088439e2e8f87fcfec1df3656b2cb55
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Citations in the corpus
- Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023, background): “Microglia phagocytose misfolded proteins, cellular debris, and dying cells to maintain homeostasis.(2) Additionally, microglia could monitor and protect neuronal functions through microglia-neuron crosstalk.”
- The Amyloid-β Pathway in Alzheimer’s Disease (2021, background): “Moreover, the dysregulation of microglia activity, including that from dystrophic microglia, may be a trigger and an aggravating factor of the seeding of aberrant protein aggregates in the brain [235, 236].”