EventsMOL2NET'15, Conference on Molecular, Biomed., Comput. & Network Science and Engineering, 1st ed.
Published
This submission belongs to the session 03. USEDAT-01: USA-Europe Data Analysis Training Congress, Cambridge, UK-Bilbao, Spain-Miami, USA, 2015 of the event MOL2NET'15, Conference on Molecular, Biomed., Comput. & Network Science and Engineering, 1st ed.
Published date
04 Dec, 2015
Citation
Francisco Javier Aguirre-Crespo, Francisco Javier Prado Prado, Jan-carlo Miguel Díaz-González, Xerardo García-Mera, New theoretical model for the study of new β-secretase inhibitors, in Proceedings of MOL2NET'15, Conference on Molecular, Biomed., Comput. & Network Science and Engineering, 1st ed., 5 December–15 December 2015, MDPI: Basel, Switzerland, doi: 10.3390/MOL2NET-1-e011
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New theoretical model for the study of new β-secretase inhibitors

Francisco Javier Aguirre-Crespo 1
1. Biomedical Sciences Department, Health Science Division, University of Quintana Roo
2. Department of Organic Chemistry, University of Santiago de Compostela, 15782, Spain.
Abstract

Alzheimer's disease (AD) is the most prevalent form of dementia, and current indications show that twenty-nine million people live with AD worldwide, a figure expected rise exponentially over the coming decades. AD is characterize with several pathologies this disease, amyloid plaques, composed of the β-amyloid peptide and γ-amyloid peptide are hallmark neuropathological lesions in Alzheimer's disease brain. Indeed, a wealth of evidence suggests that β-amyloid is central to the pathophysiology of AD and is likely to play an early role in this intractable neurodegenerative disorder. For this reason, we developed a new QSAR (QSAR) model to discover new drugs. A public databases ChEMBL contain Big Data sets of inhibitors of β-secretase. We revised QSAR studies using method of Artificial Neural Network (ANN) in order to understand the essential structural requirement for binding with receptor for β-secretase inhibitors.

Keywords
QSAR
β-secretase inhibitors
Alzheimer's disease (AD)
Manuscript
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