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Background <p>Treatment-resistant schizophrenia (TRS) affects approximately 30% of patients with schizophrenia, with clozapine remaining the most effective treatment despite its limitations. Recent evidence suggests that neuroinflammation plays a crucial role in TRS pathophysiology, with altered immune responses and elevated inflammatory markers contributing to disease progression. Understanding these mechanisms may open new avenues for therapeutic interventions.</p> Objective <p>This review aims to consolidate the current knowledge on neuroinflammation in TRS and explore emerging immune-modulating treatment options.</p> Methods <p>A systematic literature review was conducted, including studies published between 2000 and 2024 on neuroinflammation and treatment strategies for TRS. Databases such as PubMed and SCOPUS were searched using key terms including “schizophrenia,” “treatment-resistant schizophrenia,” “inflammation,” “neuroinflammation,” and “therapy.” Only studies involving human subjects and demonstrating clinical improvement were considered.</p> Results <p>Several immune-modulating treatments show promise for TRS. N-acetylcysteine (NAC) may reduce oxidative stress and modulate glutamatergic transmission, improving negative symptoms. Celecoxib, a COX-2 inhibitor, has shown mixed results, with some studies reporting symptom improvement, particularly in acute psychosis. Aspirin, a non-selective COX inhibitor, demonstrated benefits in early-stage schizophrenia. Minocycline, an antibiotic with anti-inflammatory properties, exhibited improvements in negative symptoms and cognitive function. Biological therapies such as tocilizumab (IL-6 receptor inhibitor), rituximab (B-cell depleting antibody), and canakinumab (IL-1β inhibitor) have shown variable efficacy, with limitations due to blood–brain barrier penetration.</p> Conclusion <p>Neuroinflammation plays a key role in TRS, and immune-modulating treatments may offer alternative therapeutic strategies. While preliminary findings are promising, larger, well-controlled studies are necessary to determine their clinical relevance and long-term effects. Future research should focus on personalized approaches targeting inflammatory pathways in TRS patients.</p>

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Neuroinflamation Treatment Options in Resistant Schizophrenia—State of the Art

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月20日

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  • Zoé Correia Sá,
  • André Buinho,
  • Teresa Oliveira,
  • Francisca Ribeirinho Soares,
  • João Paulo Rema,
  • Filipa Novais

摘要

Background

Treatment-resistant schizophrenia (TRS) affects approximately 30% of patients with schizophrenia, with clozapine remaining the most effective treatment despite its limitations. Recent evidence suggests that neuroinflammation plays a crucial role in TRS pathophysiology, with altered immune responses and elevated inflammatory markers contributing to disease progression. Understanding these mechanisms may open new avenues for therapeutic interventions.

Objective

This review aims to consolidate the current knowledge on neuroinflammation in TRS and explore emerging immune-modulating treatment options.

Methods

A systematic literature review was conducted, including studies published between 2000 and 2024 on neuroinflammation and treatment strategies for TRS. Databases such as PubMed and SCOPUS were searched using key terms including “schizophrenia,” “treatment-resistant schizophrenia,” “inflammation,” “neuroinflammation,” and “therapy.” Only studies involving human subjects and demonstrating clinical improvement were considered.

Results

Several immune-modulating treatments show promise for TRS. N-acetylcysteine (NAC) may reduce oxidative stress and modulate glutamatergic transmission, improving negative symptoms. Celecoxib, a COX-2 inhibitor, has shown mixed results, with some studies reporting symptom improvement, particularly in acute psychosis. Aspirin, a non-selective COX inhibitor, demonstrated benefits in early-stage schizophrenia. Minocycline, an antibiotic with anti-inflammatory properties, exhibited improvements in negative symptoms and cognitive function. Biological therapies such as tocilizumab (IL-6 receptor inhibitor), rituximab (B-cell depleting antibody), and canakinumab (IL-1β inhibitor) have shown variable efficacy, with limitations due to blood–brain barrier penetration.

Conclusion

Neuroinflammation plays a key role in TRS, and immune-modulating treatments may offer alternative therapeutic strategies. While preliminary findings are promising, larger, well-controlled studies are necessary to determine their clinical relevance and long-term effects. Future research should focus on personalized approaches targeting inflammatory pathways in TRS patients.