Abstract
Alzheimer׳s disease (AD) is one of the most common dementias showing slow progressive cognitive decline. Progression of intracerebral 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.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia
AD may be characterized by progressive intra-cerebral accumulation of beta amyloid (Aβ) peptides [5]
It is of interest to evaluatethe importance of fisetin binding with AD associated AChE, Amyloid binding alcohol dehydrogenase (ABAD) and BACE1 proteins using molecular docking and analysis
Summary
Alzheimer’s disease (AD) is the most common form of dementia. It is a harmful neurological disorder that affects the aged people that is increasing substantially with the symptoms of memory loss, decaylanguage and problems with visual spatial search [1, 2]. Amyloid binding alcohol dehydrogenase (ABAD), a mitochondrial enzyme responsible for mitochondrial dysfunction and in the pathogenesis of AD is known [8]. The application and use of molecular docking analysis in predicting ligand-protein target is well established in recent years [32].
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