Omics analysis of mouse brain models of human diseases

• Published in: Gene 2017-02, Vol.600, p.90-100
• Main Authors: 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
• Format: Article
• Language: English
• Subjects: Amyloidosis; Animals; Autism; Behavior, Animal; Brain Diseases - genetics; Brain Diseases - metabolism; Cognitive science; Cognitive Sciences; Disease Models, Animal; Gene Expression Profiling; Gene Regulatory Networks; Genomics - methods; Humans; Huntington; Life Sciences; Male; Mental Disorders - genetics; Mental Disorders - metabolism; Metabolic Networks and Pathways; Mice; Mice, Knockout; Mice, Transgenic; Network; Neurobiology; Neurodegenerative Diseases - genetics; Neurodegenerative Diseases - metabolism; Neurons and Cognition; Neuroscience; Parkinson; Proteomic; Proteomics - methods; Psychology; Psychology and behavior; Schizophrenia; Tauopathy; Transcriptomic
• ISSN: 0378-1119; 1879-0038
• DOI: 10.1016/j.gene.2016.11.022

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 few major biological processes indicating that brain diseases of diverse aetiologies might utilize common biological pathways in the nervous system, without necessarily involving similar molecules. •A common molecular signature does not exist across brain diseases.•Only one major common function exists across brain diseases.•Hubs/bottlenecks represented