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अमूर्त

Bioinformatic Analysis of Alzheimer’s Disease Using Functional Protein Sequences

Allam Appa Rao, Kiran Kumar Reddi and Hanuman Thota

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by deposition of amyloid plaques composed of aggr e- gated amyloid beta plaques, and neurofibrillary tangles composed of hyperphosphorylated tau that leads to synaptic defects resu lting in neuritic dystrophy and neuronal death. Missense mutations in amyloid precursor protein (APP), PS-1 (presenilin-1 situated on chromosome 14), PS-2 (presenilin-2 situated on chromosome 1) genes alter the proteolysis of APP and increase the generation of Aâ42 (amyloid â-42). The accumulation of Aâ42 as diffuse plaques triggers the inflammatory responses in the form of microglial activ ation and release of cytokines. In addition, perturbation of equilibrium between kinases and phosphatases results in hyperphosporylat ion of tau protein. These events culminate in neuronal degeneration and neuronal loss.

In the present study, we extracted huge amounts of data from various biological databases available online. It is found that th ere are 74 genes that may cause Alzheimer’s disease .We evaluated the role of 74 proteins that are likely to be involved in Alzheimer’s di sease by employing multiple sequence alignment using ClustalW tool and constructed a Phylogenetic tree using functional protein sequence s extracted from NCBI. Phylogenetic tree was constructed using Neighbour – Joining Algorithm in Bioinformatics approach. The results of this study suggest that PS-1, PS-2, and APP have a dominant role in the pathogenesis of Alzheimer’s disease. The pre sent study raises the possibility that genetic components are more important in Alzheimer’s disease compared to environmental, metab olic, and age related factors.