Abstract
Depletion of acetylcholine in the central nervous system (CNS) is responsible for memory loss and cognition deficit. Enzyme acetylcholinesterase (AChE) is responsible for destruction of acetylcholine (Ach) in the brain. Many herbal plant extracts have been investigated for their potential use in the treatment of Alzheimer’s disease (AD) by inhibiting AChE and upregulating the levels of Ach. The current study investigated the anti-acetylcholinesterase (AChE) activity of an aqueous extract of Unicaria tomentosa bark which has not been reported so far in the literature. The in vitro study of an aqueous extract of U. tomentosa showed maximum inhibition of 76.2±0.002 % at 0.4mg/ml of final concentration with an IC50 = 0.112 mg/ml. The mechanism of inhibition was elucidated by kinetic study which showed mixed type of inhibition, this might be due to the presence of various phytoconstituents such as oxindole alkaloids present in an aqueous extract. Based on molecular structure of phytoconstituents obtained from U. tomentosa known from the relevant literature, in-silico molecular docking study was performed against AChE protein to validate the results.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease and the most common form of dementia afflicting approximately 35 million people worldwide [1]
The clinical symptoms associated with AD include impaired ability to learn new information and recall old information, a decline in language function, dyspraxia, agnosia and impairment of executive functioning [3]
The current therapeutic strategies mainly involve focusing on anti-cholinesterase inhibitors
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease and the most common form of dementia afflicting approximately 35 million people worldwide [1]. Neuropathological changes include neuronal reduction, neurofibrillary tangles, senile neurotic plaques and a variable amyloid angiopathy [4]. Neurochemical changes occur, including a marked reduction in the levels of acetylcholine and other neurotransmitters and neuromodulators [5]. Several mechanisms have been proposed to explain the cause of the disease including those of the misfolded and aggregated proteins of amyloid beta and tau [6]. The most conventional theory is “cholinergic hypothesis”. This hypothesis proposes that there is decline in concentration of the neurotransmitter, acetylcholine (Ach) mainly due to the action of cholinesterase enzymes in CNS [7, 8]. The current therapeutic strategies mainly involve focusing on anti-cholinesterase inhibitors
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