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Microglial inflammation and phagocytosis in Alzheimer's disease: Potential therapeutic targets
Sohaib Nizami1, Hazel Hall-Roberts1,2, Sharat Warrier1,2
1Alzheimer's Research UK Oxford Drug Discovery Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Abstract:
One of the largest unmet medical needs is a disease-modifying treatment for Alzheimer's disease (AD). Recently, the role of microglia in disease, particularly AD, has gained great interest, following the identification of several disease risk-associated genes that are highly expressed in microglia. Microglia play a critical homeostatic role in the brain, with neuroinflammatory and phagocytic mechanisms being of particular importance. Here, we review the role of NLRP3, the complement system, and the triggering receptor expressed in myeloid cells 2 (TREM2) in modulating microglial functions. We have reviewed the targets, their molecular pathways and the therapeutic interventions aimed at modulating these targets, in the hope of discovering a novel therapeutic approach for the treatment of AD. LINKED ARTICLES: This article is part of a themed section on Therapeutics for Dementia and Alzheimer's Disease: New Directions for Precision Medicine. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.18/issuetoc.
Insights
Researchers explored microglia
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia are crucial for brain homeostasis, with neuroinflammation and phagocytosis being key functions.
- Alzheimer's disease (AD) research increasingly focuses on microglia due to risk genes.
- NLRP3, complement system, and TREM2 are central to microglial function in AD.
Purpose of the Study:
- To review the roles of NLRP3, complement system, and TREM2 in microglial function.
- To examine molecular pathways and therapeutic targets for modulating these microglial components.
- To identify novel therapeutic strategies for Alzheimer's disease.
Main Methods:
- Literature review of studies on microglia, NLRP3, complement system, and TREM2 in AD.
- Analysis of molecular pathways implicated in microglial function.
- Evaluation of therapeutic interventions targeting identified pathways.
Main Results:
- NLRP3, complement system, and TREM2 significantly influence microglial activity in AD.
- Specific molecular pathways involving these targets have been identified.
- Various therapeutic interventions are being explored to modulate these targets.
Conclusions:
- Modulating NLRP3, complement system, and TREM2 offers potential for novel AD therapeutics.
- Targeting microglial pathways represents a promising direction for disease-modifying treatments.
- Further research into these targets could lead to effective Alzheimer's disease treatments.