Background

A review examines the mechanisms by which microglia-centered neuroinflammation contributes to the onset and progression of neurodegenerative diseases, along with related treatment challenges. The paper by Saini and Dhiman, published in Molecular Biology Reports, covers components of neuroinflammation, biomarker candidates, computational models, and therapeutic approaches. It does not report new experiments or treatment efficacy in patients.

Inflammation in the central nervous system has traditionally been understood as a protective immune response. Evidence is accumulating, however, that persistent activation of microglia, astrocytes, and peripheral immune pathways contributes to neurodegeneration and synapse loss. The review considers Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, examining the role of neuroinflammation in each. Reviewing several diseases does not mean that they share identical mechanisms or treatment responses.

Key findings

The review focuses on microglial activation, astrocyte responses, infiltration of peripheral immune cells, cytokine dysregulation, and blood–brain barrier (BBB) damage. This approach considers neuroinflammation as a phenomenon involving intertwined immune responses inside and outside the brain and changes in the barrier, rather than as a problem involving microglia alone. The review also addresses the role of neuroinflammation in acute neurological symptoms and mental and cognitive dysfunction.

Candidate biomarkers for disease diagnosis and monitoring include markers of glial activation, inflammatory cytokines, BBB-related proteins, and kynurenine-pathway metabolites. The provided abstract, however, gives no accuracy estimates, measurement conditions, or performance by patient group for individual tests. Describing a candidate as promising must be distinguished from establishing that it has been validated for clinical use.

The review also discusses the potential of mathematical and systems-level computational models as tools for explaining complex interactions between the nervous and immune systems and predicting disease course and treatment outcomes. The abstract describes these possible uses but does not report the development methods or predictive performance of any specific model. It is therefore difficult to interpret this discussion as reporting model validation performed by the review authors themselves.

Significance and outlook

Therapeutic approaches reviewed include anti-inflammatory and immunomodulatory drugs, lifestyle interventions, stem-cell approaches, gene editing, and nanoparticle-based drug delivery. This list reflects current and future research directions targeting neuroinflammation. It should not be interpreted as evidence establishing the efficacy of a specific drug in patients or the prospects for approval of a gene-editing therapy. The magnitude of treatment effects and the clinical development stage of individual treatments also cannot be determined from the provided abstract alone.

The authors note that translating preclinical findings into effective clinical treatments remains difficult. They present advances in integrated neuroimmune modeling, biomarker-based treatment, and precision medicine as potential routes toward individualized treatment plans. The review’s significance lies in examining possible connections among neuroinflammatory mechanisms, disease monitoring, and therapeutic development, and in outlining challenges to clinical translation, rather than in providing new evidence of treatment efficacy.

Source: Review abstract and bibliographic information indexed in Europe PMC. Article DOI: 10.1007/s11033-026-12128-8.