Title

Authors

Affiliation

¹Department of Pharmacy, BGC Trust University Bangladesh, Chittagong-4000, Bangladesh; ²Department of Biochemistry and Molecular Biology, University of Chittagong, Chittagong-4331, Bangladesh; ³Department of Pharmacy, University of Chittagong, Chittagong-4331, Bangladesh; ⁴Subject Teacher, Department of Biology and Human Biology, Chittagong Grammar School (CGS), Sarson Road, AskarDiggi, Chittagong-4000, Bangladesh

Email

talhabmb@gmail.com; *Corresponding author

Article Type

Hypothesis

Date

Received August 24, 2014; Revised September 09, 2014; Accepted September 11, 2014; Published September 30, 2014

Alzheimer’s disease (AD) is one of the most common dementias showing slow progressive cognitive decline. Progression of intra-cerebral accumulation of beta amyloid (Aβ) peptides by the action of amyloid binding alcohol dehydrogenase (ABAD), a mitochondrial enzyme and β-site amyloid precursor protein cleaving enzyme 1 (BACE1) and the degradation of Acetylcholinesterase (AChE) the main pathological characteristics of AD. Therefore, it is of interest to evaluate the importance of fisetin (a flavonol that belongs to the flavonoid group of polyphenols) binding with AChE, ABAD and BACE1 proteins. Docking experiment of fisetin with these proteins using two different tools namely iGEMDOCK and FlexX show significant binding with acceptable binding values. Thus, the potential inhibitory role of fisetin with AD associated proteins is documented. 

Citation

Dash et al.   Bioinformation 10(9): 562-568(2014)
 

Edited by

P Kangueane

ISSN

0973-2063

Publisher

Biomedical Informatics

License

This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.