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Updated: Dec 21, 2025
Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
Published on: November 9, 2018
The age-related microglial transformation in Alzheimer's disease pathogenesis
Chunxu Yuan1, Ailikemu Aierken1, Zhen Xie1
1Key Laboratory of Molecular Medicine and Biotherapy, Department of Biological Sciences, School of Life Science, Beijing Institute of Technology, Beijing, China.
Abstract:
Neuroinflammatory responses mediated by microglia, the resident immune cells of the central nervous system, have long been a subject of study in the field of Alzheimer's disease (AD). Microglia express a wide range of receptors that act as molecular sensors, through which they can fulfill their various functions. In this review, we first analyzed the changes in the expression levels of microglial membrane receptors SR-A, TREM2, CD36, CD33, and CR3 in aging and AD and described the different roles of these receptors in amyloid-beta clearance and inflammatory responses. Two classical hallmarks of AD are extracellular amyloid-beta deposits and intracellular aggregated phosphorylated tau. In AD, microglia reaction was initially thought to be triggered by amyloid deposits. New evidence showed it also associated with increased phosphorylation of tau. However, which first appeared and induced activated microglia is not clear. Then we summarized diverse opinions on it. Besides, as AD is tightly linked to aging, and microglia changes dramatically on aging, yet the relative impacts of both aging and microglia are less frequently considered, so at last, we discussed the roles of aging microglia in AD. We hope to provide a reference for subsequent research.
Insights
Microglia
Area of Science:
- Neuroscience
- Immunology
- Gerontology
Background:
- Microglia, the central nervous system's immune cells, play a crucial role in Alzheimer's disease (AD) pathogenesis.
- Their function is modulated by various membrane receptors involved in sensing and responding to AD hallmarks.
- Aging significantly alters microglial characteristics, impacting their role in AD.
Purpose of the Study:
- To review changes in microglial receptor expression (SR-A, TREM2, CD36, CD33, CR3) during aging and AD.
- To elucidate the roles of these receptors in amyloid-beta clearance and neuroinflammation.
- To discuss the interplay between aging, microglia, and AD, and the sequence of pathological events.
Main Methods:
- Literature review and synthesis of existing research on microglial receptors in AD and aging.
- Analysis of changes in receptor expression levels and their functional consequences.
- Discussion of current hypotheses regarding the initiation of microglial activation in AD.
Main Results:
- Specific microglial receptors (SR-A, TREM2, CD36, CD33, CR3) show altered expression in aging and AD.
- These receptors are implicated in both amyloid-beta clearance and the modulation of inflammatory responses.
- The precise trigger for microglial activation in AD (amyloid-beta vs. tau) remains debated.
Conclusions:
- Understanding microglial receptor dynamics is key to deciphering AD neuroinflammation.
- Aging microglia exhibit distinct profiles that significantly influence AD progression.
- Further research is needed to clarify the causal relationships between aging, tau/amyloid pathology, and microglial activation in AD.
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