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Updated: May 21, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Manipulation of microglial activity as a therapy for Alzheimer's disease
Bobby Tan1, Rachel Huiyi Choi, Tammy Jing Yee Chin
1Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Abstract:
The review aims to elucidate the potential of microglia as a therapeutic target in alleviating Alzheimer's Disease (AD). Microglia are the resident immune cells in the brain which respond to the presence of the hallmarks of AD, amyloid-beta (A beta) plaques and neurofibrillary tangles (NFT). Activated microglia are able to phagocytose and secrete pro-inflammatory and anti-inflammatory cytokines. However, the eventual accumulation of excess A beta peptides and NFT in AD means that microglial clearance of pathogens has been impaired. Pro-inflammatory cytokines may also contribute to the neurodegeneration. Based on the amyloid cascade hypothesis, A beta-activated microglia can produce pro-inflammatory cytokines which may exacerbate the hyperphosporylation of tau proteins that forms NFT in AD pathology. Microglial activation can thus be manipulated to prevent neurodegeneration and promote neuroprotection through several therapeutic agents and methods. Further studies regarding comprehensive microglial response towards A beta and NFT are required to develop an effective treatment of AD involving microglia.
Insights
Targeting microglia, the brain's immune cells, shows promise for Alzheimer's Disease (AD) treatment. Modulating microglial responses to amyloid-beta and neurofibrillary tangles could prevent neurodegeneration and enhance neuroprotection.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia are brain-resident immune cells responding to Alzheimer's Disease (AD) hallmarks: amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFT).
- Activated microglia phagocytose and secrete cytokines, but impaired clearance and excessive inflammation contribute to AD pathology.
Purpose of the Study:
- To review the therapeutic potential of targeting microglia for Alzheimer's Disease (AD) alleviation.
- To explore how microglial activation influences AD pathogenesis and neurodegeneration.
Main Methods:
- Literature review synthesizing current understanding of microglial function in AD.
- Analysis of the amyloid cascade hypothesis and microglial involvement in tau hyperphosphorylation.
Main Results:
- Microglial dysfunction, characterized by impaired Aβ clearance and pro-inflammatory cytokine release, exacerbates AD.
- Therapeutic manipulation of microglial activation presents a viable strategy for neuroprotection.
Conclusions:
- Modulating microglial responses to Aβ and NFT is a promising therapeutic avenue for AD.
- Further research into comprehensive microglial responses is crucial for developing effective AD treatments targeting these cells.
