Verapamil attenuates scopolamine induced cognitive deficits by averting oxidative stress and mitochondrial injury – A potential therapeutic agent for Alzheimer’s Disease

Ponne, Saravanaraman; Chinnadurai, Raj Kumar; Boopathy, Rathanam

doi:10.1007/s11011-019-00498-x

Cited by 20 publications

(19 citation statements)

References 75 publications

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“…Results of this study revealed that the administration of scopolamine reduced percentage alternation in Y‐maze, and increased escape latency in MWM tasks. This result supports previous studies that scopolamine induces cognitive impairment in animals (Hashimoto, Hatayama, Nakamichi, & Yoshida, 2014; Klinkenberg & Blokland, 2010; Kwon, Kim, Lee, & Jang, 2009; Ponne, Kumar, & Boopathy, 2020). However, pretreatment with A. paniculata extract and donepezil reversed the increase in escape latency and a decline in memory function caused by scopolamine administration.…”

Section: Discussionsupporting

confidence: 92%

Effect of Andrographis paniculata leaves extract on neurobehavioral and biochemical indices in scopolamine‐induced amnesic rats

et al. 2020

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The brain plays a major role in the central nervous system (CNS) and an important organ of the body that controls the functions of all other organs with the aid of neurons through signal transmission, whereas, in neurodegeneration, the functions of these neurons are impaired or altered (Ortman, Velkoff, & Hogan, 2014). Neurodegeneration is a process that refers to any pathology that mainly affects the neurons gradually. This condition alters the structure and function of neurons which leads to increased neuronal death, poor decision making, loss

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Section: Discussionsupporting

confidence: 92%

Effect of Andrographis paniculata leaves extract on neurobehavioral and biochemical indices in scopolamine‐induced amnesic rats

et al. 2020

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“…Oxidative stress has also been proposed as the possible cause of neurocognitive disease along with the cholinergic hypothesis. Regarding the use of scopolamine, previous studies have reported the association of systemic administration of scopolamine with increased oxidative stress in the brain, especially the areas associated with memory and learning, such as the hippocampus and prefrontal cortex, some of which are reported to be involved in mitochondrial dysfunction 15,32 . Furthermore, scopolamine-induced memory impairment is successfully attenuated by several anti-oxidant compounds, emphasizing the crucial role of oxidative stress in scopolamine-induced amnesia 14,33 .…”

Section: Discussionmentioning

confidence: 99%

Scopolamine-Induced Delirium Promotes Neuroinflammation and Neuropsychiatric Disorder in Mice

Cheon

Koo

Kim

et al. 2020

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Postoperative delirium is a common neuropsychiatric syndrome resulting a high postsurgical mortality rate and decline in postdischarge function. Extensive research has been performed on both human and animal delirium models due to their clinical significance, focusing on systematic inflammation and consequent neuroinflammation playing a key role in the pathogenesis of postoperative cognitive dysfunctions. Since animal models are widely utilized for pathophysiological study of neuropsychiatric disorders, this study aimed at examining the validity of the scopolamine-induced delirium mice model with respect to the neuroinflammatory hypothesis of delirium. Male C57BL/6 mice were treated with intraperitoneal scopolamine (2 mg/kg). Neurobehavioral tests were performed to evaluate the changes in cognitive functions, including learning and memory, and the level of anxiety after surgery or scopolamine treatment. The levels of pro-inflammatory cytokines (IL-1ꞵ, IL-18, and TNF-α) and inflammasome components (NLRP3, ASC, and caspase-1) in different brain regions were measured. Gene expression profiles were also examined using whole-genome RNA sequencing analyses to compare gene expression patterns of different mice models.Scopolamine treatment showed significant increase in the level of anxiety and impairments in memory and cognitive function associated with increased level of pro-inflammatory cytokines and NLRP3 inflammasome components. Genetic analysis confirmed the different expression patterns of genes involved in immune response and inflammation and those related with the development of the nervous system in both surgery and scopolamine-induced mice models. The scopolamine-induced delirium mice model successfully showed that analogous neuropsychiatric changes coincides with the neuroinflammatory hypothesis for pathogenesis of delirium.

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“…Oxidative stress has also been proposed as the possible cause of neurocognitive disease along with the cholinergic hypothesis. Regarding the use of scopolamine, previous studies have reported the association of systemic administration of scopolamine with increased oxidative stress in the brain, especially the areas associated with memory and learning, such as the hippocampus and prefrontal cortex, some of which are reported to be involved in mitochondrial dysfunction (16,37,38). Furthermore, scopolamine-induced memory impairment is successfully attenuated by several anti-oxidant compounds, emphasising the crucial role of oxidative stress in scopolamine-induced amnesia (39,40).…”

Section: Discussionmentioning

confidence: 99%

Scopolamine-induced Delirium Promotes Neuroinflammation and Neuropsychiatric Disorder in Mice

Cheon

Koo

Kim

et al. 2020

Preprint

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BackgroundPostoperative delirium is a common neuropsychiatric syndrome resulting in a high postsurgical mortality rate and decline in postdischarge function. Extensive research has been performed on both human and animal delirium models due to their clinical significance, focusing on systemic inflammation and consequent neuroinflammation playing a key in the pathogenesis of postoperative cognitive dysfunctions. Since animal models are widely utilized for pathophysiological study of neuropsychiatric disorders, this study aimed at examining the validity of the scopolamine-induced delirium mice model with respect to the neuroinflammatory hypothesis of delirium. MethodsMale C57BL/6 mice were treated with intraperitoneal scopolamine (2 mg/kg). Neurobehavioural tests were performed to evaluate the changes in cognitive functions, including learning and memory, and the level of anxiety after surgery or scopolamine treatment. The levels of pro-inflammatory cytokines (IL-1ꞵ, IL-18, and TNF-α) and inflammasome components (NLRP3, ASC, and caspase-1) in different brain regions were measured. Gene expression profiles were also examined using whole-genome RNA sequencing analyses to compare gene expression patterns of different mice models.Results Scopolamine treatment showed significant increase in the level of anxiety and impairments in memory and cognitive function associated with increased level of pro-inflammatory cytokines and NLRP3 inflammasome components. Genetic analysis confirmed the different expression patterns of the genes involved in immune response and inflammation and those related with the development of the nervous system in both surgery and scopolamine-induced mice models. Conclusions The scopolamine-induced delirium mice model successfully showed that analogous neuropsychiatric changes coincide with the neuroinflammatory hypothesis for pathogenesis of delirium.

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Verapamil attenuates scopolamine induced cognitive deficits by averting oxidative stress and mitochondrial injury – A potential therapeutic agent for Alzheimer’s Disease

Cited by 20 publications

References 75 publications

Effect of Andrographis paniculata leaves extract on neurobehavioral and biochemical indices in scopolamine‐induced amnesic rats

Effect of Andrographis paniculata leaves extract on neurobehavioral and biochemical indices in scopolamine‐induced amnesic rats

Scopolamine-Induced Delirium Promotes Neuroinflammation and Neuropsychiatric Disorder in Mice

Scopolamine-induced Delirium Promotes Neuroinflammation and Neuropsychiatric Disorder in Mice

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