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Updated: May 7, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Potential drugs targeting microglia: current knowledge and future prospects
Parakalan Rangarajan1, Ling Eng-Ang, S Thameem Dheen
1Department of Anatomy, The Yong Loo Lin School of Medicine, National University of Singapore, Md10, 4 Medical Drive, Singapore. thameem_dheen@nuhs.edu.sg.
Abstract:
Inflammation in the central nervous system (CNS) may occur as a result of trauma, infection or neurodegenerative stimuli and is characterized by activation of microglia, the resident immune cells of the CNS. Activated microglia proliferate rapidly, migrate to the site of injury or infection and elicit immune response by phagocytosis of cell debris, production of cytokines, chemokines and reactive oxygen species, and presentation of antigens to other immune cells. In addition, microglia participate in tissue repair by producing neurotrophic factors. However, when microglia are chronically activated, they become neurotoxic to the surrounding CNS parenchyma. Chronic activation of microglia has been shown to augment neurodegeneration in Parkinson's disease (PD), Alzheimer's disease (AD), brain injury and number of other CNS pathologies. Identification of factors that control microglial activation, therefore, has become the major focus of recent research. A number of herbal and chemical compounds have been shown to attenuate microglial activation. However, these compounds exhibit non-specificity and produce unpleasant side-effects. Here, we provide a comprehensive review on some of the currently available drugs known to reduce microglial activation, their molecular targets and the subcellular signaling networks on which they act. We also review some of the newly emerging therapeutic avenues such as 'epidrugs' and finally emphasize on the importance of targeted drug delivery systems for alleviating microglia-mediated neurotoxicity.
Insights
Microglia activation drives neuroinflammation and neurodegeneration in CNS diseases. This review covers drugs targeting microglia activation, their molecular mechanisms, and novel therapeutic strategies for neuroprotection.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Central nervous system (CNS) inflammation involves microglia, the resident immune cells.
- Microglia activation is crucial in injury response but chronic activation causes neurotoxicity, exacerbating neurodegenerative diseases like Parkinson's and Alzheimer's.
- Controlling microglial activation is a key research focus for treating CNS pathologies.
Purpose of the Study:
- To review current drugs that reduce microglial activation.
- To explore their molecular targets and signaling pathways.
- To discuss emerging therapies like epidrugs and targeted drug delivery for neuroprotection.
Main Methods:
- Comprehensive literature review of existing drugs and novel therapeutic approaches.
- Analysis of molecular targets and subcellular signaling networks involved in microglial activation.
- Evaluation of targeted drug delivery systems for CNS applications.
Main Results:
- Several compounds can attenuate microglial activation, but often lack specificity and cause side effects.
- Understanding molecular targets and signaling pathways is crucial for developing effective treatments.
- Emerging strategies like epidrugs and targeted delivery show promise for mitigating neurotoxicity.
Conclusions:
- Targeting microglial activation is essential for managing neuroinflammation and neurodegeneration.
- Further research into specific molecular pathways and advanced drug delivery is needed.
- Developing targeted therapies can improve treatment efficacy and reduce side effects in CNS disorders.
