Editorial - Journal of Experimental Stroke & Translational Medicine (2025) Volume 17, Issue 2
Neuroinflammation: Mechanisms, Clinical Implications, and Therapeutic Perspectives
Sophia Bennett*
Department of Neuroscience, Faculty of Medicine, University of Sydney, Australia
- *Corresponding Author:
- Sophia Bennett
Department of Neuroscience, Faculty of Medicine, University of Sydney, Australia
E-mail: sophia.bennett@usyd.edu.au
Received: 01-March-2025, Manuscript No. jestm-25-170396; Editor assigned: 3-March-2025, PreQC No. jestm-25-170396 (PQ); Reviewed: 17-March-2025, QC No. jestm-25-170396; Revised: 24-March-2025, Manuscript No. jestm-25-170396 (R); Published: 31-March-2025, DOI: 10.37532/jestm.2024.16(6).321-322
Introduction
Neuroinflammation refers to the inflammatory response within the central nervous system (CNS), involving activation of resident immune cells such as microglia and astrocytes, along with infiltration of peripheral immune cells. While inflammation is a natural defense mechanism [1], its persistence in the CNS can disrupt neuronal homeostasis and contribute to neurodegeneration. Neuroinflammation has been increasingly recognized as a key pathological feature in a wide spectrum of neurological disorders, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, traumatic brain injury, and stroke. Understanding its underlying mechanisms is crucial for developing targeted therapies to prevent long-term neurological damage.
Mechanisms of Neuroinflammation
The CNS has traditionally been considered an “immune-privileged” site due to the protective role of the blood–brain barrier (BBB). However [2], advances in research have demonstrated robust neuroimmune interactions.
Microglial Activation: Microglia, the brain’s resident macrophages, act as the first responders to injury or infection. Upon activation, they release pro-inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6), reactive oxygen species (ROS), and nitric oxide. Although essential for pathogen defense, sustained activation promotes neuronal apoptosis and synaptic dysfunction.
Astrocytic Response: Astrocytes regulate synaptic transmission and maintain the BBB. During neuroinflammation, they become “reactive astrocytes,” producing cytokines, chemokines, and matrix metalloproteinases that can either protect or damage neural tissue depending on the context [3].
Blood–Brain Barrier Dysfunction: Inflammatory mediators weaken the BBB, allowing infiltration of T cells, B cells, and monocytes. This perpetuates a vicious cycle of inflammation and neurotoxicity.
Peripheral Immune Crosstalk: Systemic infections and chronic inflammatory conditions can exacerbate neuroinflammation via circulating cytokines and immune cell trafficking.
Clinical Implications
Persistent neuroinflammation plays a central role in the pathogenesis and progression of several neurological disorders:
Neurodegenerative Diseases: Chronic inflammation contributes to amyloid plaque deposition in Alzheimer’s disease and dopaminergic neuronal death in Parkinson’s disease.
Demyelinating Disorders: In multiple sclerosis, autoreactive T cells and inflammatory cytokines mediate demyelination and axonal loss.
Acute CNS Injury: Following traumatic brain injury or ischemic stroke, neuroinflammation can exacerbate secondary damage, leading to poor functional recovery.
Psychiatric Disorders: Growing evidence suggests that altered neuroimmune signaling is associated with depression, schizophrenia, and autism spectrum disorders.
Diagnosis
Although challenging, several biomarkers and imaging modalities are under investigation:
Neuroimaging: Positron emission tomography (PET) using ligands for translocator protein (TSPO) provides insights into microglial activation [4].
Fluid Biomarkers: Elevated levels of cytokines, chemokines, and glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) and blood may serve as indicators of neuroinflammatory activity.
Electrophysiological Changes: Alterations in EEG patterns may indirectly reflect neuroimmune dysfunction.
Therapeutic Perspectives
Targeting neuroinflammation represents a promising avenue for therapeutic intervention.
Anti-inflammatory Agents: Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids have shown limited benefit, partly due to poor CNS penetration.
Biological Therapies: Monoclonal antibodies targeting cytokines such as IL-1β and TNF-α are under evaluation.
Neuroprotective Compounds: Agents such as minocycline and resveratrol exhibit anti-inflammatory and antioxidant properties [5].
Lifestyle Interventions: Regular exercise, dietary modifications, and stress reduction have been associated with reduced neuroinflammatory markers.
Precision Medicine Approaches: Personalized therapies targeting specific immune pathways hold promise for optimizing outcomes.
Conclusion
Neuroinflammation is a double-edged sword: while essential for defense and repair, its persistence drives neurodegeneration and worsens outcomes in neurological disorders. Advances in imaging, biomarkers, and therapeutic strategies are gradually unraveling its complexity. Future approaches integrating precision medicine, lifestyle interventions, and targeted biological therapies hold promise for mitigating neuroinflammation and improving long-term neurological health.
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