Omics analysis of mouse brain models of human diseases
Abstract
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.