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Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease
Wen-Ying Wang1, Meng-Shan Tan1, Jin-Tai Yu1
11 Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao 266071, China ; 2 Department of Neurology, Qingdao Municipal Hospital, College of Medicine and Pharmaceutics, Ocean University of China, Qingdao 266071, China ; 3 Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing 210006, China.
Abstract:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the brain, which is characterized by the formation of extracellular amyloid plaques (or senile plaques) and intracellular neurofibrillary tangles. However, increasing evidences demonstrated that neuroinflammatory changes, including chronic microgliosis are key pathological components of AD. Microglia, the resident immune cells of the brain, is constantly survey the microenvironment under physiological conditions. In AD, deposition of β-amyliod (Aβ) peptide initiates a spectrum of cerebral neuroinflammation mediated by activating microglia. Activated microglia may play a potentially detrimental role by eliciting the expression of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) influencing the surrounding brain tissue. Emerging studies have demonstrated that up-regulation of pro-inflammatory cytokines play multiple roles in both neurodegeneration and neuroprotection. Understanding the pro-inflammatory cytokines signaling pathways involved in the regulation of AD is crucial to the development of strategies for therapy. This review will discuss the mechanisms and important role of pro-inflammatory cytokines in the pathogenesis of AD, and the ongoing drug targeting pro-inflammatory cytokine for therapeutic modulation.
Insights
Alzheimer's disease involves neuroinflammation, with microglia activating and releasing pro-inflammatory cytokines like IL-1β. Understanding these cytokine pathways is key for developing new Alzheimer's disease therapies.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Alzheimer's disease (AD) is characterized by amyloid plaques and neurofibrillary tangles.
- Neuroinflammation, particularly chronic microgliosis, is increasingly recognized as a key pathological component of AD.
- Microglia, the brain's immune cells, become activated by amyloid-beta (Aβ) deposition, initiating neuroinflammation.
Purpose of the Study:
- To review the mechanisms and roles of pro-inflammatory cytokines in Alzheimer's disease pathogenesis.
- To discuss the dual roles of pro-inflammatory cytokines in neurodegeneration and neuroprotection.
- To explore therapeutic strategies targeting pro-inflammatory cytokines for AD modulation.
Main Methods:
- This review synthesizes existing research on neuroinflammation in Alzheimer's disease.
- It examines the signaling pathways of key pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α.
- The review discusses current and emerging drug targets related to these cytokines.
Main Results:
- Activated microglia release pro-inflammatory cytokines, contributing to AD pathology.
- These cytokines have complex roles, potentially mediating both neurodegeneration and neuroprotection.
- Dysregulation of cytokine signaling is central to the progression of Alzheimer's disease.
Conclusions:
- Pro-inflammatory cytokines are critical players in Alzheimer's disease pathogenesis.
- Targeting cytokine signaling pathways offers a promising avenue for therapeutic intervention in AD.
- Further understanding of these pathways is essential for developing effective treatments.
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