Mice lacking BCAS1, a novel myelin‐associated protein, display hypomyelination, schizophrenia‐like abnormal behaviors, and upregulation of inflammatory genes in the brain. Issue 5 (23rd February 2017)

• Record Type: Journal Article
• Authors: Ishimoto, Tetsuya; Ninomiya, Kensuke; Inoue, Ran; Koike, Masato; Uchiyama, Yasuo; Mori, Hisashi
• Is Part Of: Glia. Volume 65:Issue 5(2017)
• Page Start: 727
• Page End: 739
• Publication Date: 2017-02-23
• Subjects: oligodendrocyte -- Schwann cells -- schizophrenia -- knockout mouse -- hypomyelination; Neuroglia -- Periodicals; Neurology -- Periodicals; 611.0188
• DOI: 10.1002/glia.23129
• Languages: English
• ISSNs: 0894-1491

Abstract

Abstract: The abnormal expression and function of myelin‐related proteins contribute to nervous system dysfunction associated with neuropsychiatric disorders; however, the underlying mechanism of this remains unclear. We found here that breast carcinoma amplified sequence 1 (BCAS1), a basic protein abundant in the brain, was expressed specifically in oligodendrocytes and Schwann cells, and that its expression level was decreased by demyelination. This suggests that BCAS1 is a novel myelin‐associated protein. BCAS1 knockout mice displayed schizophrenia‐like behavioral abnormalities and a tendency toward reduced anxiety‐like behaviors. Moreover, we found that the loss of BCAS1 specifically induced hypomyelination and the expression of inflammation‐related genes in the brain. These observations provide a novel insight into the functional link between oligodendrocytes and inflammation and/or abnormal behaviors. Main Points: Mice lacking BCAS1, a novel myelin‐associated protein, display schizophrenia‐like abnormal behaviors, hypomyelination, and up‐regulation of inflammatory genes in the brain. BCAS1 may be the link between myelin function and inflammation and/or abnormal behaviors.