[Redox and microglia in the pathophysiology of schizophrenia]

Takahiro A Kato1, Fuminori Hyodo, Mayumi Yamato

  • 1Innovation Center for Medical Redoz Navigation, Kyushu University; 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, 2. Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan..

Insights

Schizophrenia involves altered brain antioxidant status, with microglia playing a key role. Targeting microglia may offer new therapeutic strategies for this neurological disorder.

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Context:

  • Schizophrenia is linked to oxidative stress and altered antioxidant status in the brain.
  • Microglia, the brain's immune cells, are implicated due to their role as major superoxide radical sources.
  • Evidence suggests microglial activation and pathology in schizophrenia patients and animal models.

Purpose:

  • To review the evidence implicating microglia in schizophrenia.
  • To propose a hypothesis that microglia are critical players in schizophrenia.
  • To highlight microglia as a potential therapeutic target for schizophrenia.

Summary:

  • Altered antioxidant status is observed in schizophrenia.
  • Microglia activation and pathology are evident in schizophrenia.
  • Antipsychotics can directly impact microglia, inducing proinflammatory reactions and oxidative stress.
  • Minocycline, a microglial inhibitor, shows therapeutic effects in schizophrenia.
  • Modulating microglia represents a novel therapeutic avenue for schizophrenia.

Impact:

  • This review proposes a novel hypothesis linking microglia to schizophrenia.
  • It suggests that targeting microglia could lead to new schizophrenia treatments.
  • In vivo molecular redox imaging is proposed as a tool to validate this hypothesis.

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