Micro(glial)-managing executive function: white matter inflammation drives catatonia
Sarah E. Pease-Raissi and Jonah R. Chan
Department of Neurology and UCSF Weill Institute for Neuroscience, UCSF, San Francisco, California, USA.
Address correspondence to: Sarah E. Pease-Raissi, University of California, San Francisco, Sandler Neurosciences Center, 675 Nelson Rising Lane, Room 260, Box 3206, San Francisco, California 94158, USA. Phone: 415.353.4390; Email: sarah.raissi@ucsf.edu.
Find articles by Pease-Raissi, S. in: JCI | PubMed | Google Scholar
Department of Neurology and UCSF Weill Institute for Neuroscience, UCSF, San Francisco, California, USA.
Address correspondence to: Sarah E. Pease-Raissi, University of California, San Francisco, Sandler Neurosciences Center, 675 Nelson Rising Lane, Room 260, Box 3206, San Francisco, California 94158, USA. Phone: 415.353.4390; Email: sarah.raissi@ucsf.edu.
Find articles by Chan, J. in: JCI | PubMed | Google Scholar
First published December 18, 2017 - More info
J Clin Invest. 2018;128(2):564–566. https://doi.org/10.1172/JCI98761.
Copyright © 2018, American Society for Clinical Investigation
White matter abnormalities are prevalent in neuropsychiatric disorders such as schizophrenia, but it is unclear whether these abnormalities represent a cause or consequence of these disorders. Reduced levels of the myelin protein 2′-3′-cyclic nucleotide 3′-phosphodiesterase (CNP) are associated with the schizophrenic symptom catatonia in both humans and mouse models. In this issue of the JCI, Janova et al. show that reduced CNP levels correlate with catatonia and white matter inflammation in human subjects. Furthermore, they demonstrate that microglial ablation prevents and alleviates catatonic signs in Cnp–/– mice, indicating that microglial-mediated inflammation causes catatonia. Together, this study identifies a cellular mechanism by which subtle myelin abnormalities cause low-grade neuroinflammation and catatonic behavior.
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