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