Abstract

Crinum macowanii has been found to contain alkaloids that have activity against acetylcholinesterase enzyme in vitro. The present study was undertaken to investigate the in vivo ability of hydroethanolic crude extract of Crinum macowanii to ameliorate memory impairment induced by scopolamine. Thirty-six male Balb/c mice weighing around 25–35 g were employed in the present investigation. Y-maze and novel object recognition apparatus served as the exteroceptive behavioural models, and scopolamine-induced amnesia served as the interoceptive behavioural model. C. macowanii (10, 20, and 40 mg/kg p.o.) was administered in single doses to the mice. Donepezil (3 mg/kg p.o.) was used as a positive control agent. C. macowanii extract reversed the amnesia induced by scopolamine as indicated by a dose-dependent increase in spontaneous alternation performance in the Y-maze task. C. macowanii 40 mg/kg showed significant activity (p < 0.05 versus negative control), comparable to that of the positive control. C. macowanii also showed memory-enhancing activity against scopolamine-induced memory deficits in the long-term memory novel object recognition performance as indicated by a dose-dependent increase in the discrimination index. The results indicate that the hydroethanolic extract of C. macowanii may be a useful memory restorative mediator in the treatment of cognitive disorders such as Alzheimer's disease.

Highlights

  • Dementia is a general term for the loss of memory and other intellectual abilities serious enough to disrupt daily activities later in life [1]

  • There was a dose-dependent increase in the percentage of spontaneous alternation performance (%SAP) among Crinum macowanii (CM) treated groups (Figure 1(d)). %SAP for the CM40 mg/kg group was high, comparable to that of the positive control group (DPZ3 mg/kg + Scop)

  • A significant difference was observed between the CM40 mg/kg + Scop and Scop1 mg/kg groups (p < 0.01). %SAP between the Scop1 mg/kg and the vehicle and positive controls group had significant differences (p < 0.05)

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Summary

Introduction

Dementia is a general term for the loss of memory and other intellectual abilities serious enough to disrupt daily activities later in life [1]. AD is a progressive neurodegenerative disease of the brain characterized by memory loss, behavioural changes, and associative signs and symptoms [4]. The most accepted therapeutic approach in AD has been the use of acetylcholinesterase inhibitors (AChEIs). This blocks the activity of an enzyme called acetylcholinesterase which normally breaks down acetylcholine (ACh). Inhibition of this enzyme prevents the breakdown of ACh that is known to be lacking in the AD brain. Selective AChEIs, free of dose-limiting side effects, are until now not available Taking into account these therapeutic limitations of AD, there is a compelling need to discover and develop new and better drugs for this devastating disorder

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