Abstract:Abstract. In the present study, we assessed the effect of the ethanolic extract of the seeds of Cassia obtusifolia (COE) on the learning and memory impairments induced by scopolamine or transient bilateral common carotid artery occlusion (2VO). In a study of the cholinergic dysfunction induced by scopolamine, single COE (25, 50, or 100 mg / kg, p.o.) administration significantly attenuated scopolamine-induced cognitive impairments as determined by the passive avoidance and Y-maze tasks (P<0.05) and also reduce… Show more
“…Cholinergic agents include ACh precursors, which increase the synthesis of ACh; nicotinic or M1 muscarinic agonists, which directly stimulate cholinergic receptors or allosterically modulate nAChR [41] ; and synaptic AChE inhibitors, which prevent the degradation of ACh. Recent preclinical and clinical evidence indicates that treatment with cholinergic agents has beneficial effects on dementia of vascular origin [42][43][44][45][46][47][48] .…”
Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning
confidence: 99%
“…Methanesulfonyl fluoride (MSF), a highly selective CNS inhibitor of AChE, has recently been demonstrated to promote improvement in cognitive performance in patients with AD [124] , and it was also shown to attenuate simple learning and memory deficits in the MCAO rat model [16] . The seed extract of Cassia obtusifolia (COE), which has been found to inhibit AChE activity both in vitro and ex vivo, attenuated memory impairment induced by scopolamine or BCCAO in the passive-avoidance, Y-maze, and Morris water-maze tests in ICR mice [47] . Another agent that could increase ChAT activity and inhibit AChE activity is Z-Ligustilide (LIG).…”
Vascular dementia (VaD) is a progressive neurodegenerative disease with a high prevalence. Several studies have recently reported that VaD patients present cholinergic deficits in the brain and cerebrospinal fluid (CSF) that may be closely related to the pathophysiology of cognitive impairment. Moreover, cholinergic therapies have shown promising effects on cognitive improvement in VaD patients. The precise mechanisms of these cholinergic agents are currently not fully understood; however, accumulating evidence indicates that these drugs may act through the cholinergic anti-inflammatory pathway, in which the efferent vagus nerve signals suppress pro-inflammatory cytokine release and inhibit inflammation, although regulation of oxidative stress and energy metabolism, alleviation of apoptosis may also be involved. In this paper, we provide a brief overview of the cholinergic treatment strategy for VaD and its relevant mechanisms of anti-inflammation.
“…Cholinergic agents include ACh precursors, which increase the synthesis of ACh; nicotinic or M1 muscarinic agonists, which directly stimulate cholinergic receptors or allosterically modulate nAChR [41] ; and synaptic AChE inhibitors, which prevent the degradation of ACh. Recent preclinical and clinical evidence indicates that treatment with cholinergic agents has beneficial effects on dementia of vascular origin [42][43][44][45][46][47][48] .…”
Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning
confidence: 99%
“…Methanesulfonyl fluoride (MSF), a highly selective CNS inhibitor of AChE, has recently been demonstrated to promote improvement in cognitive performance in patients with AD [124] , and it was also shown to attenuate simple learning and memory deficits in the MCAO rat model [16] . The seed extract of Cassia obtusifolia (COE), which has been found to inhibit AChE activity both in vitro and ex vivo, attenuated memory impairment induced by scopolamine or BCCAO in the passive-avoidance, Y-maze, and Morris water-maze tests in ICR mice [47] . Another agent that could increase ChAT activity and inhibit AChE activity is Z-Ligustilide (LIG).…”
Vascular dementia (VaD) is a progressive neurodegenerative disease with a high prevalence. Several studies have recently reported that VaD patients present cholinergic deficits in the brain and cerebrospinal fluid (CSF) that may be closely related to the pathophysiology of cognitive impairment. Moreover, cholinergic therapies have shown promising effects on cognitive improvement in VaD patients. The precise mechanisms of these cholinergic agents are currently not fully understood; however, accumulating evidence indicates that these drugs may act through the cholinergic anti-inflammatory pathway, in which the efferent vagus nerve signals suppress pro-inflammatory cytokine release and inhibit inflammation, although regulation of oxidative stress and energy metabolism, alleviation of apoptosis may also be involved. In this paper, we provide a brief overview of the cholinergic treatment strategy for VaD and its relevant mechanisms of anti-inflammation.
“…The Morris water maze task was carried out as described elsewhere (Kim et al, 2007). On the following day, acquisition and retrieval session were conducted (Fig.…”
− Several lines of evidence indicate that scopolamine as a nonselective muscarinic antagonist disrupts object recognition performance and spatial working memory when administered systemically. In the present study, we investigated the different effects of scopolamine on acquisition, consolidation, and retrieval phases of object recognition performance and spatial working memory using the object recognition and the Morris water maze tasks in mice. In the acquisition phase test, scopolamine decreased recognition index on object recognition task and the trial 1 to trial 2 differences on Morris water maze task. In the consolidation and retrieval phase tests, scopolamine also decreased recognition index on object recognition task, where as scopolamine did not exhibited any effects on the Morris water maze task.
“…In addition, a loss of forebrain cholinergic neurons, reduction in acetylcholine level in the cerebral cortex and hippocampus in Alzheimer's Disease. A defect in cholinergic transmission led to the development of acetylcholinesterase (AChE) inhibitors to treat dementia associated with Alzheimer's Disease 4 .…”
In the present study, we studied the effects of the ethanol extract of Commiphora berryi bark on drug-induced learning and memory-impaired mice using Y-maze task and passive avoidance task. On pretreatment with the ethanol extract of Commiphora berryi at 100mg/Kg p.o significantly ameliorated scopolamine-induced cognitive impairments which were revealed by the reversal in the reduction of spontaneous alteration in the Y -maze task and by significant improvement in latency time in passive avoidance task. This confirms the presence of bioactive phytoconstituents in Commiphora berryi which could be useful to decline the cognitive deficits in memory-impaired mice.
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