Kudo, Noriko Osaka University
Yamamori, Hidenaga Osaka University
Ishima, Tamaki Chiba University
Nemoto, Kiyotaka University of Tsukuba
Yasuda, Yuka Osaka University
Fujimoto, Michiko Osaka University
Azechi, Hirotsugu Osaka University
Niitsu, Tomihisa Chiba University
Ikeda, Manabu Osaka University
Iyo, Masaomi Chiba University
Fukunaga, Masaki National Institute for Physiological Sciences
Watanabe, Yoshiyuki Osaka University
Hashimoto, Kenji Chiba University
Hashimoto, Ryota Osaka University
soluble tumor necrosis factor receptor 2
Background: An imbalance in the inflammatory tumor necrosis factor system, including soluble tumor necrosis factor receptor 2 (sTNFR2), may contribute to the pathophysiology of schizophrenia.
Methods: We measured the plasma levels of sTNFR2 in 256 healthy controls and 250 patients with schizophrenia including antipsychotic drug-free patients and treatment-resistant patients. We also explored the possible association between plasma sTNFR2 levels and cognitive performance in healthy controls and patients with schizophrenia using the Wechsler Adult Intelligence Scale, Third Edition, the Wechsler Memory Scale-Revised, and the Rey Auditory Verbal Learning Test. An association between plasma sTNFR2 levels and hippocampal volume in controls and patients with schizophrenia was also investigated via MRI.
Results: We found that the plasma levels of sTNFR2 were significantly higher in patients with schizophrenia, including both antipsychotic drug-free patients and treatment-resistant patients. We found a significant negative association between plasma sTNFR2 levels and cognitive performance in controls and patients with schizophrenia. Hippocampal volume was also negatively associated with plasma sTNFR2 levels in patients with schizophrenia.
Conclusion: Together, these convergent data suggest a possible biological mechanism for schizophrenia, whereby increased sTNFR2 levels are associated with a smaller hippocampal volume and cognitive impairment.
International Journal of Neuropsychopharmacology
Oxford University Press
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