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<p>Neuroinflammation is a multifaceted and carefully regulated process within the central nervous system (CNS) that serves a dual function in both protecting neurons and contributing to neurodegenerative processes. This process is mainly driven by activated microglia, astrocytes, and immune cells that infiltrate in response to neuronal damage, infections, or toxic exposures. This review emphasizes the key molecular pathways involved in neuroinflammatory reactions, such as the JAK/STAT, NF-κB, NLRP3 inflammasome, and MAPK signaling pathways. Each of these pathways plays a role in the generation and release of pro-inflammatory substances that maintain and increase inflammation in the CNS. Furthermore, the review examines the significance of crucial pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) as well as the chemokines CCL2 and CXCL10, which coordinate the recruitment of immune cells and contribute to neuronal injury. Gaining an understanding of the interactions among these signaling pathways and mediators sheds light on the molecular mechanisms connected to various neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Targeting these inflammatory signaling networks may provide valuable therapeutic approaches to manage neuroinflammation and avert its long-lasting neurotoxic effects.</p>

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A mechanistic insight of neuro-inflammation signaling pathways and implication in neurodegenerative disorders

  • 期刊论文

  • 发表日期：

    2025年11月21日

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  • Amina Shafi,
  • Mariam Akmal,
  • Aisha Sethi,
  • Zunera Chauhdary

摘要

Neuroinflammation is a multifaceted and carefully regulated process within the central nervous system (CNS) that serves a dual function in both protecting neurons and contributing to neurodegenerative processes. This process is mainly driven by activated microglia, astrocytes, and immune cells that infiltrate in response to neuronal damage, infections, or toxic exposures. This review emphasizes the key molecular pathways involved in neuroinflammatory reactions, such as the JAK/STAT, NF-κB, NLRP3 inflammasome, and MAPK signaling pathways. Each of these pathways plays a role in the generation and release of pro-inflammatory substances that maintain and increase inflammation in the CNS. Furthermore, the review examines the significance of crucial pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) as well as the chemokines CCL2 and CXCL10, which coordinate the recruitment of immune cells and contribute to neuronal injury. Gaining an understanding of the interactions among these signaling pathways and mediators sheds light on the molecular mechanisms connected to various neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Targeting these inflammatory signaling networks may provide valuable therapeutic approaches to manage neuroinflammation and avert its long-lasting neurotoxic effects.