This review highlights neuroinflammation's dual impact on neurodegenerative diseases, indicating potential therapeutic targets for treatment.
Neuroinflammation, an immune response within the central nervous system (CNS), plays a dual role in brain health—acting as both a protective mechanism and a contributor to neurodegeneration when chronically activated. Triggered by various factors including infections, trauma, toxic metabolites, and autoimmunity, neuroinflammation involves activation of glial cells and release of proinflammatory molecules such as cytokines and reactive oxygen species. While acute neuroinflammation may support tissue repair, prolonged inflammation can lead to neuronal damage and contribute to the progression of multiple neurodegenerative diseases. This report explores the pathological and clinical interconnection between neuroinflammation and disorders such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis (ALS), Multiple Sclerosis (MS), and Multiple System Atrophy (MSA). Each disease displays distinct clinical and neuropathological features, yet shares overlapping mechanisms involving immune dysregulation, protein aggregation, and glial activation. Current therapeutic strategies focus on targeting these pathways to halt or slow disease progression. Despite existing drug therapies offering symptomatic relief, there remains an urgent need for disease-modifying treatments. Emerging research emphasizes multi-target drug approaches, early diagnostic biomarkers, and personalized medicine as future directions in combating neurodegenerative disorders driven by neuroinflammation.
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Kumar et al. (2025) studied this question.
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