A Computational approach to uncover the missense mutations in candidate genes of late-onset Alzheimer’s disease

Abstract

Abstract Background Alzheimer’s (induced by ultimate demise of nerve cells) is a neurodegenerative disorder, and experts are still lagging in this disease, owing to the polygenic and multi-factorial nature mainly in Late-Onset-Alzheimer’s-Disease (LOAD). Till now, Amyloid beta (Aβ) aggregation along with neuroinflammation seem to be the main inveterate attribute of Alzheimer’s Disease (AD). Hence, and intriguing area of research that motivates the researchers is to incorporate genes implicated in Aβ clearance and associated regulatory processes. Aim of study: The principle purpose of the present study, is to investigate neuro-inflammatory and A cleavage genes (ADAM10, CD33, & TNFSF10). Methodology: Assessment of missense mutations of Aβ cleavage genes was done, and their effects were evaluated, followed by analysing the gene-gene and protein-protein interactions. Further, the association of Aβ targeting drugs with genes of investigation was examined. Also, Docking was applied to identify clinical involvement of therapeutic targets. Result the results proved that the underlying mechanism and polymorphism in just one nucleotide was related to the disease. It also provides useful information about genes’ network, that contain targeting molecules of NOTCH signalling and Death Induced Signalling Complex (DISC) pathway. Future Directions : The research will be valuable to find new directions for therapeutic approaches, with more benefit and success rate in disease treatment.