Homology Modeling and in silico docking analysis of BDNF in the treatment of Alzheimer's disease
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Alzheimer's disease (AD) is a progressive, degenerative disorder that affects the brain's nerve cells or neurons resulting in memory loss, thinking and behavorial changes. This neurodegenerative disorder affects the neurons of the brain by forming plaques and tangles. There is no effective drug or cure for Alzheimer's disease. There is hope in the potential of stem cells to help us learn and understand about the mechanisms underlying this devastating neurodegenerative disease. From neural stem cell research, it is identified that the protein neurotrophin enhances the level of neurotrophin which will aid in the treatment of neurodegenerative disease. This protein possesses BDNF (brain derived neurotrophic factor) that plays an important role in the process of neurogenesis. The objective of the present study is to evaluate the effect of BDNF and its interaction with the selected ligands in the treatment of Alzheimer's disease. Homology modeling was done for protein BDNF using Modeller v9.13 and the modeled structure was validated using PROCHECK server. A total of 8 ligands such as Citalopram, Ampakines, Fingolimodphosphate, Donepezil, Memantine, Rasogiline, Fluoxetine and Cystamine were taken for docking analysis. The active site prediction was done using CASTP program. Docking analysis was done using Arguslab and the interactions were visualized using PyMol. Fingolimod phosphate showed the least binding energy with the maximum hydrogen bond interactions. The ligand FTY720P had six hydrogen bond interactions where 47ASN binds with 711N….3927O with distance of 2.985Å, 25ASN binds with 391N….3928O with distance of 2.352Å, 4LEU binds with 3906N….56O with distance 2.999Å, 7THR binds with 3906N….114O with distance 2.999 Å, 8MET39290…128O with distance 2.8109Å and 7THR 3929O….114O distance 2.8817Å. Hence, Fingolimodphosphate could be a potent drug and therefore further in vitro studies could be carried out which would play an important role in reducing the effect of AD.
Neurotrophin, BDNF, Alzheimer's disease, Homology Modeling, Arguslab, docking.