According to World Health Organization estimation about 18 million people worldwide are suffering from Alzheimer's disease (AD) and figures would shoot up to 34 million by 2025 in aging population. The onset and propagation of AD is unrelenting from cellular to molecular levels, governed by multitude of factors leading to a continual decrease in cognitive abilities (Felsenstein et al., 2014). Recent advances in understanding the genetic factors that predispose to AD, as well as in biomarker development have brought with them the promise of earlier and more reliable diagnosis of this disease. However, treatment regime and strategies available, approved by US-FDA are limited by their scope to alter pharmacological targets that can provide symptomatic relief to the patient (Lannfelt et al., 2014). The present stock of drugs for AD consists of donepezil, galantamine, rivastigmine, and memantine. The primary mechanism of action for these drugs is to decrease the acetyl cholinesterase (AChE) levels thus altering acetylcholine level, while memantine is a low-affinity voltage-dependent uncompetitive antagonist at glutamatergic N-methyl d-aspartate receptor (NMDA) thereby blocking the activity of the neurotransmitter glutamate. All the existing treatments for AD are only symptomatic but non curative (Lannfelt et al., 2014). Under these circumstances a drug molecule with multiple pharmacological properties with intent to modify as well as reduce the risk factors contributing toward disease burden will be highly appreciated. Drugs that are aimed at disrupting AD disease progression by inhibition/degradation of the protein mis-folding of β-amyloid (Aβ) into neurotoxic oligomeric aggregates has been encouraged for AD (Scheff et al., 2007).