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.

白质异常在精神分裂症等神经精神疾病中普遍存在，但尚不清楚这些异常是这些疾病的起因还是后果。在人类和小鼠模型中，髓磷脂蛋白2'-3'-环核苷酸3'-磷酸二酯酶（CNP）水平的降低与精神分裂症的症状性卡塔尼亚有关。在JCI的这一期中，Janova等人。研究表明，降低的CNP水平与人类受试者的卡塔尼亚和白质发炎有关。此外，他们证明了小胶质细胞消融可以预防和减轻Cnp-/-小鼠的阳离子症状，表明小胶质细胞介导的炎症会导致卡塔顿症。总之，这项研究确定了一种细胞机制，通过该机制，细微的髓磷脂异常会导致轻度神经炎症和紧张行为。