Mice lacking BCAS1, a novel myelin-associated protein, display hypomyelination, schizophrenia-like abnormal behaviors, and upregulation of inflammatory genes in the brain

Glia. 2017 May;65(5):727-739. doi: 10.1002/glia.23129. Epub 2017 Feb 23.


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.

Keywords: Schwann cells; hypomyelination; knockout mouse; oligodendrocyte; schizophrenia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / metabolism*
  • Brain / pathology
  • Demyelinating Diseases / genetics*
  • Demyelinating Diseases / pathology
  • Inflammation / genetics
  • Mice, Knockout
  • Myelin Basic Protein / genetics
  • Myelin Basic Protein / metabolism
  • Myelin Sheath / metabolism
  • Myelin Sheath / pathology
  • Neoplasm Proteins / deficiency
  • Neoplasm Proteins / metabolism*
  • Oligodendroglia / metabolism*
  • Schizophrenia / genetics
  • Schizophrenia / pathology
  • Transcriptional Activation / genetics
  • Up-Regulation


  • Bcas1 protein, mouse
  • Myelin Basic Protein
  • Neoplasm Proteins