Targeting Neutrophil Extracellular Traps in Neuroinflammation: A Therapeutic Perspective on Neurodegenerative Diseases.
Targeting Neutrophil Extracellular Traps in Neuroinflammation: A Therapeutic Perspective on Neurodegenerative Diseases.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Alfenas, BR · Author affiliation
Multicenter Postgraduate Program in Physiological Sciences, Department of Physiological Sciences, Institute of Biomedical Sciences, Federal University of Alfenas, Alfenas 37133-840, MG, Brazil.Location evidence
Ribeirão, BR · Author affiliation
Center for Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto 14040-900, SP, Brazil.Location evidence
São Paulo, BR · Author affiliation
Center for Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto 14040-900, SP, Brazil.Location evidence
Ribeirão Preto, BR · Author affiliation
Center for Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto 14040-900, SP, Brazil.Location evidence
Glasgow, GB · Author affiliation
Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK.Location evidence
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Original abstract
Neuroinflammation is a complex process involved in the pathogenesis of several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, Huntington's disease, and amyotrophic lateral sclerosis. Neutrophils, although traditionally considered peripheral immune cells, have emerged as active participants in the immunopathology of the central nervous system (CNS) through the release of neutrophil extracellular traps (NETs), structures composed of decondensed chromatin embedded with pro-inflammatory proteins. Evidence suggests that NETs play a dual role: they are protective against pathogens but can also induce tissue damage when produced in excess. Several pathways are involved in their formation, including vesicle-mediated release (vital NETs), the lytic NADPH oxidase (NOX)-dependent pathway, and the mitochondrial pathway. Targeting NETs therapeutically, through the use of NETosis inhibitors, NET-degrading strategies, or blockade of neutrophil migration, has shown promise in reducing neuroinflammation/neurodegeneration and improving neurological outcomes in experimental models. This review aims to investigate both the protective and deleterious roles of NETs and how this knowledge may reveal new therapeutic strategies to modulate neurodegenerative diseases and preserve neural integrity, offering valuable insights for potential applications in clinical practice.