Identifying molecular signatures and pathways shared between Alzheimer's and Huntington's disorders: A bioinformatics and systems biology approach

Abstract

Alzheimer's disease and Huntington's disease are considered to be the most lethal illnesses that result in common human disorders. Alzheimer's disease (AD) is a progressive neurological illness distinguished by age-related dementia, mental abnormalities, and poor memory, among other symptoms. However, Huntington's disease (HD) is influenced by genetics as well as a generalized dysfunction of the motor system. Despite the fact that many similar genetic elements have been found in the literature as being interrelated between these two diseases, it is still unclear how people acquire infected with these two neurological disorders. Detecting biomarkers for Alzheimer's and Huntington's disease in brain tissue might help in drug development and treatment. The purpose of this research was to find brain cell transcripts that show levels of gene expression linked to the progression of Alzheimer's and Huntington's disease. A bioinformatics pipeline was used to study one RNA-Seq transcriptomic dataset and one microarray dataset, and 24 significant differentially expressed genes (DEGs) were discovered that were shared by two brain cell datasets. We uncovered disease-gene association networks and signaling pathways, as well as gene ontology (GO) investigations and hub protein identification, to determine the roles of these DEGs. The discovery of significant gene ontologies and molecular pathways increased our understanding of the pathophysiology of these two disorders, and the hub proteins B2M, HLA-A, HLA-E, HLA-B, HLA-C, HLA-F, CANX, HLA-DQA1, HLA-DRA, and HLA-DRB1 might be exploited to design therapeutic interventions. In neurological disorder subjects, we uncovered efficient hypothetical linkages between pathogenic processes in brain cells, implying that brain cells may be exploited to detect and monitor illness origin and development, as well as design pharmacological therapies.