News Releases & Research Results Elucidation of the pathogenic mechanism of oxidative stress in schizophrenia: discovery of protein dysfunction associated with carbonyl stress in schizophrenia

News Releases & Research Results

Outline

Results of the joint research conducted by Project Professor Nobutaka Hirokawa of Graduate School of Medicine, University of Tokyo and Team Leader Takeo Yoshikawa of the RIKEN center for Brain Science.
 

Key points of research results

  • In schizophrenia associated with carbonyl stress (*1) disease pathology was shown for the first time to be potentially based on loss of cytoskeletal control function due to multimerization of carbonyl-modified CRMP2 protein (*2).
    *1: Accumulation of advanced glycogen end products resulting from modification of proteins, sugars, and/or lipids nonenzymatically mediated by reactive carbonyl compounds affected by oxidative stress.
    *2: A type of microtubule associated protein, predominantly present in neuronal cells
  • The association between carbonyl stress and schizophrenia is unknown; however, a new molecular pathway was detected using iPS cells derived from patients and structural analysis at the atomic level.
  • These results are expected to support the development of molecular targeting therapy, drug discovery, and prophylaxes for schizophrenia.

This research was supported by Strategic Research Program for Brain Sciences of AMED.

These results were published in Life Science Alliance, dated October 7.

Article

Toyoshima M., et al. Enhanced carbonyl stress induces irreversible multimerization of CRMP2 in schizophrenia pathogenesis, Life Science Alliance
DOI:10.26508/lsa.201900478

2019.10.7

Last updated 2019.10.7