Abstract
Alzheimer's disease is a major neurodegenerative illness whose prevalence is increasing worldwide but the molecular mechanism remains unclear. There is some scientific evidence that the molecular complexity of Alzheimer's pathophysiology is associated with the formation of extracellular amyloid-beta plaques in the brain. A novel cross- phenotype association analysis of imaging genetics reported a brain atrophy susceptibility gene, namely FAM222A and the protein Aggregatin encoded by FAM222A interacts with amyloid-beta (A?)-peptide (1-42) through its N-terminal A? binding domain and facilitates A? aggregation. The function of Aggregatin protein is unknown, and its three-dimensional structure has not been analyzed experimentally yet. Our goal was to investigate the interaction of Aggregatin with A? in detail by in silico analysis, including the 3D structure prediction analysis of Aggregatin protein by homology modeling. Our analysis verified the interaction of the C-terminal domain of model protein with the N-terminal domain of A?. This is the first attempt to demonstrate the interaction of Aggregatin with the A?. These results confirmed in vitro and in vivo study reports claiming FAM222A helping to ease the aggregating of the A?-peptide.
Highlights
Alzheimer’s disease (AD) is observed as a widespread and incurable ailment worldwide because of the elevated average human lifespan in recent years
This research seeks to address the association of Aggregatin protein, whose function and three-dimensional structure is not characterized yet, with Alzheimer’s pathology using in silico analysis
Even though Aggregatin is expressed in the nerve cells, it remains uncertain from which part of the cell and compartment it is released and how it forms a core with the extracellular amyloid-beta plaques
Summary
Alzheimer’s disease (AD) is observed as a widespread and incurable ailment worldwide because of the elevated average human lifespan in recent years. The elevation of AD patient number in the population has become a social and an economic problem as an AD patient becomes dependent on another person.[1,2] The global number of AD patients who have dementia was estimated to be 43·8 million worldwide[3] and over 5 million in the USA. Through the middle of the century, this number may dramatically increase in the USA to 13.8 million people with Alzheimer’s dementia.[4]. It is unclear what the exact function of APP is, its role in cell growth and biological activities including signal transduction and neuronal development has been shown in several studies.[7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
