Monday, 17 October 2016

Selenoergothionein as a Potential Inhibitor against Amyloid β-Protein (Aβ): Docking and Molecular Dynamics Studies

Alzheimer‘s disease (AD) is a progressive neurodegenerative disorder, encircling the deterioration of cognitive functions and behavioral changes, characterized by the aggregation of amyloid β-protein (Aβ) into fibrillar amyloid plaques in elected areas of the brain with the lipid-carrier protein apolipoprotein E (apoE), the microtubule associated protein tau, and the presynaptic protein α-synuclein. 

Amyloid β-Protein
High levels of fibrillary Aβ, the main constituent of senile plaques, are deposited in the AD brain that outcome in the thrashing of synapses, neurons and destruction of neuronal role. Aβ is derived from the amyloid precursor protein through sequential protein cleavage by as partylprotease, β-secretase and presenilin-dependent β-secretase triggering a spill of events such as oxidative damage, neurotoxicity, and inflammation that contributes to the progression of AD. Therefore the Aβ protein may be a target for anti-Alzheimer drugs. Aβ proteinwas retrieved from the Protein data bankand energy minimized and subjectedto molecular dynamic simulations using NAMD 2.9 software with CHARMM27 force field in water. 

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