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Published on: November 9, 2018
Microglia in Alzheimer's Disease: A Target for Therapeutic Intervention
Guimei Zhang1, Zicheng Wang1, Huiling Hu2
1Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Jilin University, Changchun, China.
Abstract:
Alzheimer's disease (AD) is one of the most common types of age-related dementia worldwide. In addition to extracellular amyloid plaques and intracellular neurofibrillary tangles, dysregulated microglia also play deleterious roles in the AD pathogenesis. Numerous studies have demonstrated that unbridled microglial activity induces a chronic neuroinflammatory environment, promotes β-amyloid accumulation and tau pathology, and impairs microglia-associated mitophagy. Thus, targeting microglia may pave the way for new therapeutic interventions. This review provides a thorough overview of the pathophysiological role of the microglia in AD and illustrates the potential avenues for microglia-targeted therapies, including microglial modification, immunoreceptors, and anti-inflammatory drugs.
Insights
Microglia, immune cells in the brain, are key players in Alzheimer's disease (AD) pathogenesis. Targeting these cells offers promising therapeutic strategies for AD treatment.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Alzheimer's disease (AD) is a leading cause of dementia, characterized by amyloid plaques and neurofibrillary tangles.
- Dysregulated microglia, the brain's immune cells, significantly contribute to AD pathogenesis through chronic neuroinflammation.
- Impaired microglial mitophagy exacerbates AD pathology, highlighting microglia as a critical therapeutic target.
Purpose of the Study:
- To provide a comprehensive review of the pathophysiological role of microglia in Alzheimer's disease.
- To explore potential therapeutic strategies targeting microglia for AD intervention.
Main Methods:
- Literature review of studies on microglial function in AD.
- Analysis of the impact of microglial dysregulation on AD hallmarks.
- Identification of therapeutic targets within microglial pathways.
Main Results:
- Microglial overactivation promotes neuroinflammation, amyloid-beta accumulation, and tau pathology in AD.
- Microglia-associated mitophagy dysfunction is a critical factor in AD progression.
- Targeting microglia presents a viable therapeutic avenue for Alzheimer's disease.
Conclusions:
- Microglia play a multifaceted and detrimental role in Alzheimer's disease progression.
- Therapeutic strategies focused on modulating microglial activity, immunoreceptors, and inflammation show promise for AD treatment.
- Modulating microglial function represents a significant opportunity for novel Alzheimer's disease therapies.
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