Commentary - Journal of Brain and Neurology (2025) Volume 8, Issue 1

Neuroinflammation: Mechanisms, implications, and therapeutic perspectives

Neuroinflammation: Mechanisms, implications, and therapeutic perspectives.^*

Department of Clinical Pharmacy, University of Medical Sciences, Iraq

*Corresponding Author:

Souvik Ghosh
Department of Clinical Pharmacy
University of Medical Sciences,
Iraq
E-mail: souvik@gmail.com

Received: 02-Feb-2025, Manuscript No. AAJBN-25-169531; Editor assigned: 03-Feb-2025, PreQC No. AAJBN-25-169531(PQ); Reviewed: 16-Feb-2025, QC No. AAJBN-25-169531; Revised: 20-Feb-2025, Manuscript No. AAJBN-25-169531(R); Published: 27-Feb-2025, DOI:10.35841/aajbn-8.1.185

Citation Ghosh S. Neuroinflammation: Mechanisms, implications, and therapeutic perspectives. J Brain Neurol. 2025;8(1):185

Introduction

Neuroinflammation refers to the activation of the brain’s innate immune system in response to injury, infection, or neurodegenerative processes. It is primarily mediated by microglia and astrocytes, which serve as the first line of defense in the central nervous system (CNS). While acute neuroinflammation can be protective, helping to remove harmful stimuli and repair damaged tissue, chronic neuroinflammation often leads to progressive neural damage. This dual nature makes it a critical focus in understanding various brain disorders and developing targeted treatments. [1].

The mechanisms behind neuroinflammation are complex and multifaceted. Upon detection of pathogens, toxins, or damaged cells, microglia become activated and release pro-inflammatory cytokines, chemokines, and reactive oxygen species (ROS). This response can help eliminate harmful agents but can also inadvertently harm healthy neurons if the inflammatory state persists. Astrocytes, another crucial glial cell type, contribute to the inflammatory process by releasing additional mediators and forming glial scars, which can both protect and hinder neural recovery. [2].

A major consequence of prolonged neuroinflammation is its link to neurodegenerative diseases. Conditions such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS) show strong correlations with chronic inflammatory activity in the CNS. In Alzheimer’s, for example, amyloid-beta plaques activate microglia, triggering a cycle of inflammation and neuronal damage. This persistent inflammatory state contributes to the progression of cognitive decline.[3].

In addition to neurodegenerative diseases, neuroinflammation plays a significant role in acute neurological conditions. Traumatic brain injury (TBI), stroke, and infections such as meningitis can all initiate strong inflammatory responses in the brain. While this inflammation is initially protective, unresolved or excessive responses can exacerbate damage, leading to long-term neurological deficits. The blood–brain barrier (BBB) plays a pivotal role in regulating neuroinflammation. Under normal conditions, the BBB restricts immune cell entry into the brain. However, in inflammatory states, BBB permeability increases, allowing immune cells and inflammatory molecules from the bloodstream to enter the CNS. This can amplify the inflammatory response and further disrupt neural function.[4].

Advances in neuroimaging and molecular biology have improved the ability to study neuroinflammation in living patients. Positron emission tomography (PET) scans using specific tracers can detect activated microglia, providing valuable insights into disease progression and the effects of treatment. At the molecular level, researchers are identifying biomarkers, such as specific cytokines, that could be used for early diagnosis and monitoring of inflammation-related brain disorders. Therapeutic approaches to neuroinflammation are an active area of research. Anti-inflammatory drugs, immunomodulatory therapies, and agents targeting microglial activation are being explored for their potential to halt or slow disease progression. Lifestyle interventions, including regular exercise, anti-inflammatory diets, and stress management, also appear to play a role in modulating brain inflammation.[5].

Conclusion

Neuroinflammation is a complex biological process with both protective and harmful consequences for brain health. While essential in responding to injury or infection, chronic and uncontrolled neuroinflammation contributes significantly to the pathogenesis of many neurological disorders. Understanding its mechanisms and identifying effective interventions remain critical for preventing and managing brain diseases. Ongoing research offers hope that targeted therapies will one day allow clinicians to control harmful inflammation without compromising the brain’s defense systems, ultimately improving outcomes for patients

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