Scopolamine-induced greater alterations in neurochemical profile and increased oxidative stress demonstrated a better model of dementia: A comparative study

Haider, Saida; Tabassum, Saiqa; Perveen, Tahira

doi:10.1016/j.brainresbull.2016.10.002

Cited by 88 publications

(50 citation statements)

References 56 publications

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“…Anti-muscarinic drugs, including scopolamine, are currently used to reproduce experimental models of cognitive impairments associated with neurodegenerative diseases (Haider et al, 2016). Accordingly, scopolamine administered to our mice caused them to have amnesia.…”

Section: Discussionmentioning

confidence: 99%

The impact of scopolamine pretreatment on 3-iodothyronamine (T1AM) effects on memory and pain in mice

Laurino

Lucenteforte

Siena

et al. 2017

Hormones and Behavior

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Section: Discussionmentioning

confidence: 99%

The impact of scopolamine pretreatment on 3-iodothyronamine (T1AM) effects on memory and pain in mice

Laurino

Lucenteforte

Siena

et al. 2017

Hormones and Behavior

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“…To evaluate spatial memory after 1 h of learning acquisition a probe trial was performed. During probe trial the platform was removed from its location and the rats were allowed to swim for 120 s, during this time the parameters that were assessed during probe trial included the number of entries over the target quadrant and the time spent in the target quadrant and as an index of reference/ spatial memory [33].…”

Section: Behavioral Analysismentioning

confidence: 99%

Naringenin protects AlCl3/D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress

et al. 2020

Self Cite

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Currently prescribed medications for the treatment of Alzheimer's disease (AD) that are based on acetylcholinesterase inhibition only offer symptomatic relief but do not provide protection against neurodegeneration. There appear to be an intense need for the development of therapeutic strategies that not only improve brain functions but also prevent neurodegeneration. The oxidative stress is one of the main causative factors of AD. Various antioxidants are being investigated to prevent neurodegeneration in AD. The objective of this study was to investigate the neuroprotective effects of naringenin (NAR) against AlCl 3 +D-gal induced AD-like symptoms in an animal model. Rats were orally pre-treated with NAR (50 mg/kg) for two weeks and then exposed to AlCl 3 +D-gal (150 mg/kg + 300 mg/kg) intraperitoneally for one week to develop AD-like symptoms. The standard drug, donepezil (DPZ) was used as a stimulator of cholinergic activity. Our results showed that NAR pre-treatment significantly protected AD-like behavioral disturbances in rats. In DPZ group, rats showed improved cognitive and cholinergic functions but the neuropsychiatric functions were not completely improved and showed marked histopathological alterations. However, NAR not only prevented AlCl 3 +D-gal induced AD-like symptoms but also significantly prevented neuropsychiatric dysfunctions in rats. Results of present study suggest that NAR may play a role in enhancing neuroprotective and cognition functions and it can potentially be considered as a neuroprotective compound for therapeutic management of AD in the future. PLOS ONE | https://doi.org/10.1371/journal.pone.0227631 January 16, 2020 1 / 30 OPEN ACCESS Citation: Haider S, Liaquat L, Ahmad S, Batool Z, Siddiqui RA, Tabassum S, et al. (2020) Naringenin protects AlCl 3 /D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress. PLoS ONE 15(1): e0227631.

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“…Scopolamine is a muscarinic cholinergic receptor antagonist. It is commonly used for the study of cognitive deficiency in animal models of AD [7][8][9][10][11]. Donepezil is frequently used to treat patients with mild to moderate AD.…”

Section: Introductionmentioning

confidence: 99%

Curcumin Downregulates GSK3 and Cdk5 in Scopolamine-Induced Alzheimer’s Disease Rats Abrogating Aβ40/42 and Tau Hyperphosphorylation

Das

Jana

Chakrabarti

et al. 2019

ADR

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Alzheimer's disease (AD) is the most common form of dementia. Extracellular amyloid-␤ (A␤) aggregation and tau hyperphosphorylation are the key drivers of AD. Glycogen synthase kinase 3 (GSK3) and cyclin dependent kinase 5 (Cdk5) have been known as leading applicants arbitrating abnormal tau hyperphosphorylation. Thus, we evaluated the efficacy and underlying mechanism of action of curcumin in scopolamine-induced AD rats in our study. We found that curcumin-treated AD rats markedly reduced the levels of A␤ 40 and A␤ 42 in the brain and in the plasma in comparison to untreated AD rats. Moreover, the levels of phosphorylated tau at Ser396 (PHF13), Ser202/Thr205 (AT8), and A␤ 40/42 (MOAB2) were decreased significantly in AD rats treated with curcumin. Phospho-GSK3␤ (Tyr216), the active form of GSK3␤, and total GSK3␤ were significantly decreased in AD rats treated with curcumin. Furthermore, Cdk5 and its activators p35 and p25 were significantly decreased in curcumin-treated AD rats. The reduced levels of Cdk5, p35, p25, and GSK3␤ in curcumin-treated AD rats may result decreased A␤ aggregation and tau hyperphosphorylation, thus ameliorating AD. Impaired spatial memory and locomotor activity in AD rats were partially reversed by curcumin. Therefore, curcumin, as a natural compound present in turmeric, may be a more effective therapeutic agent in the treatment of AD in humans.

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Scopolamine-induced greater alterations in neurochemical profile and increased oxidative stress demonstrated a better model of dementia: A comparative study

Cited by 88 publications

References 56 publications

The impact of scopolamine pretreatment on 3-iodothyronamine (T1AM) effects on memory and pain in mice

The impact of scopolamine pretreatment on 3-iodothyronamine (T1AM) effects on memory and pain in mice

Naringenin protects AlCl3/D-galactose induced neurotoxicity in rat model of AD via attenuation of acetylcholinesterase levels and inhibition of oxidative stress

Curcumin Downregulates GSK3 and Cdk5 in Scopolamine-Induced Alzheimer’s Disease Rats Abrogating Aβ40/42 and Tau Hyperphosphorylation

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