Abstract
Crinum macowanii is a bulbous plant indigenous to many parts of Southern Africa. Extracts of C. macowanii have gained interest since the discovery of various alkaloids, few of which possess acetylcholinesterase inhibitory activity. The present study was performed to evaluate the effect of a crude hydroethanolic extract of C. macowanii against aluminum chloride-induced memory impairment in mice using the Morris water maze and the novel object recognition task. C. macowanii (10, 20, and 40 mg/kg p.o) was administered daily for five weeks, while donepezil (3 mg/kg p.o) was used as the positive control. C. macowanii at a dosage of 40 mg/kg showed a significantly lower escape latency than the negative control (P < 0.0001) and was found to be comparable to donepezil 3 mg/kg in the Morris water maze test. C. macowanii at 40 mg/kg exhibited a significantly higher discrimination index than aluminum chloride-treated mice in the novel object recognition task. The results may support the usefulness of C. macowanii in the management of dementia and related illnesses.
Highlights
Alzheimer’s disease (AD) is a chronic neurodegenerative disease characterized by cognitive dysfunction, psychiatric, and behavioral disturbances [1]
The Morris water maze (MWM) behavioral test was utilized to assess the escape latencies (EL) and time spent in the target quadrant (TSTQ) expressed in seconds
No significant difference in EL was seen between Crinum macowanii (CM) group at 40 mg/kg and Donepezil hydrochloride (DONZ) 3 mg/kg group (P < 0 9070)
Summary
Alzheimer’s disease (AD) is a chronic neurodegenerative disease characterized by cognitive dysfunction, psychiatric, and behavioral disturbances [1]. Hallmark pathological characteristics of AD include the deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain accompanied by synaptic dysfunction [2]. This is the amyloid hypothesis, which postulates that amyloid deposits in the brain are the main cause of AD [3], while the Tau hypothesis suggests that abnormalities in the hyperphosphorylated tau protein are the cause of AD [4]. Early-onset familial Alzheimer’s disease is an uncommon form of AD caused by a mutation in one of at least three genes: PSEN1, APP gene, and PSEN2 [5]. The cholinergic hypothesis concludes that the loss of cholinergic function results in memory loss and disruption of cognitive function [7, 8]
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