Omics analysis of mouse brain models of human diseases


  • Paban Véronique
  • Loriod Béatrice
  • Villard Claude
  • Buee Luc
  • Blum David
  • Pietropaolo Susanna
  • Cho Yoon H.
  • Gory-Faure Sylvie
  • Mansour Elodie
  • Gharbi Ali
  • Alescio-Lautier Béatrice


  • Autism
  • Huntington
  • Parkinson
  • Tauopathy
  • Amyloidosis
  • Transcriptomic
  • Proteomic
  • Network
  • Schizophrenia

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The identification of common gene/protein profiles related to brain alterations, if they exist, may indicate the convergence of the pathogenic mechanisms driving brain disorders. Six genetically engineered mouse lines modelling neurodegenerative diseases and neuropsychiatric disorders were considered. Omics approaches, including transcriptomic and proteomic methods, were used. The gene/protein lists were used for inter-disease comparisons and further functional and network investigations. When the inter-disease comparison was performed using the gene symbol identifiers, the number of genes/proteins involved in multiple diseases decreased rapidly. Thus, no genes/proteins were shared by all 6 mouse models. Only one gene/protein (Gfap) was shared among 4 disorders, providing strong evidence that a common molecular signature does not exist among brain diseases. The inter-disease comparison of functional processes showed the involvement of a fewmajor biological processes indicating that brain diseases of diverse aetiologies might utilize common biological pathways in the nervous system, without necessarily involving similar molecules.

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