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Microglia in Alzheimer's Disease: A Favorable Cellular Target to Ameliorate Alzheimer's Pathogenesis
Dewan Md Sumsuzzman1, Md Sahab Uddin1,2, Md Tanvir Kabir3
1Department of Pharmacy, Southeast University, Dhaka, Bangladesh.
Abstract:
Microglial cells serve as molecular sensors of the brain that play a role in physiological and pathological conditions. Under normal physiology, microglia are primarily responsible for regulating central nervous system homeostasis through the phagocytic clearance of redundant protein aggregates, apoptotic cells, damaged neurons, and synapses. Furthermore, microglial cells can promote and mitigate amyloid β phagocytosis and tau phosphorylation. Dysregulation of the microglial programming alters cellular morphology, molecular signaling, and secretory inflammatory molecules that contribute to various neurodegenerative disorders especially Alzheimer's disease (AD). Furthermore, microglia are considered primary sources of inflammatory molecules and can induce or regulate a broad spectrum of cellular responses. Interestingly, in AD, microglia play a double-edged role in disease progression; for instance, the detrimental microglial effects increase in AD while microglial beneficiary mechanisms are jeopardized. Depending on the disease stages, microglial cells are expressed differently, which may open new avenues for AD therapy. However, the disease-related role of microglial cells and their receptors in the AD brain remain unclear. Therefore, this review represents the role of microglial cells and their involvement in AD pathogenesis.
Insights
Microglia, the brain's immune cells, are crucial for homeostasis but can worsen Alzheimer's disease (AD) pathology. Understanding their dual role is key for developing new AD therapies.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglial cells act as the brain's primary immune sensors, maintaining central nervous system homeostasis through phagocytosis.
- They are involved in clearing cellular debris, protein aggregates like amyloid-beta, and regulating tau phosphorylation.
- Microglial dysfunction is implicated in neurodegenerative diseases, particularly Alzheimer's disease (AD).
Purpose of the Study:
- To review the multifaceted role of microglial cells in the pathogenesis of Alzheimer's disease (AD).
- To elucidate how microglial dysregulation contributes to AD progression.
- To highlight the potential of targeting microglial functions for novel AD therapeutics.
Main Methods:
- Literature review focusing on microglial cell biology in the context of AD.
- Analysis of studies investigating microglial phagocytosis, inflammatory signaling, and cellular responses in AD models and patients.
- Synthesis of current understanding regarding the dual role of microglia in AD.
Main Results:
- Microglia exhibit a dual role in AD, with both beneficial and detrimental effects on disease progression.
- Dysregulated microglial activity, including altered morphology and inflammatory signaling, exacerbates AD pathology.
- Microglial expression patterns vary with disease stage, suggesting stage-specific therapeutic opportunities.
Conclusions:
- Microglial cells are central players in AD pathogenesis, exhibiting complex and context-dependent functions.
- Targeting microglial pathways represents a promising therapeutic strategy for Alzheimer's disease.
- Further research is needed to clarify the precise roles of microglial receptors and functions in the AD brain.
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