Omics analysis of mouse brain models of human diseases

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 considere...

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Bibliographic Details
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
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Summary: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
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2016.11.022