Allicin ameliorates aluminium- and copper-induced cognitive dysfunction in Wistar rats: relevance to neuro-inflammation, neurotransmitters and Aβ(1–42) analysis

Kaur, Sunpreet; Raj, Khadga; Gupta, Yamini; Singh, Shamsher

doi:10.1007/s00775-021-01866-8

Cited by 37 publications

(21 citation statements)

References 44 publications

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“…the current experiments, AlCl 3 -induced pathological changes were coupled with notable decreases in hippocampal NE, DA and 5-HT levels; this corroborates the results of former studies. 3,39 In addition, the cholinergic pathway is implicated in memory and learning. Acetylcholine is a cholinergic neurotransmitter, which is responsible for the membrane integrity of cholinergic neurons through transmembrane protein (Na + /K + -ATPase) activity.…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective efficacy of the bacterial metabolite, prodigiosin, against aluminium chloride‐induced neurochemical alternations associated with Alzheimer's disease murine model: Involvement of Nrf2/HO‐1/NF‐κB signaling

Alsharif

Albrakati

omairi

et al. 2022

Environmental Toxicology

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Prodigiosin (PDG) is a bacterial metabolite with numerous biological and pharmaceutical properties. Exposure to aluminium is considered a root etiological factor in the pathological progress of Alzheimer's disease (AD). Here, in this investigation, we explored the neuroprotective potential of PDG against aluminium chloride (AlCl 3 )mediated AD-like neurological alterations in rats. For this purpose, rats were gavaged either AlCl 3 (100 mg/kg), PDG (300 mg/kg), or both for 42 days. As a result of the analyzes performed on the hippocampal tissue, it was observed that AlCl 3 induced biochemical, molecular, and histopathological changes like those related to AD. PDG pre-treatment significantly decreased acetylcholinesterase activity and restored the levels of brain-derived neurotrophic factor, monoamines (dopamine, norepinephrine, and serotonin), and transmembrane protein (Na + /K + -ATPase). Furthermore, PDG boosted the hippocampal antioxidant capacity, as shown by the increased superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione

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Section: Discussionmentioning

confidence: 99%

“…It has been reported that the hippocampal region is enriched with cholinergic, glutaminergic, GABAergic, and monoaminergic neurotransmission and regulates memory function and processing 39 . Hence, levels of altered neurotransmitters in the hippocampus produce deficits in working memory.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective efficacy of the bacterial metabolite, prodigiosin, against aluminium chloride‐induced neurochemical alternations associated with Alzheimer's disease murine model: Involvement of Nrf2/HO‐1/NF‐κB signaling

Alsharif

Albrakati

omairi

et al. 2022

Environmental Toxicology

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“…Recently, allicin had a protective effect when administered in rats treated with aluminum chloride and copper sulfate as animal models of AD. Specifically, allicin attenuated Aβ plaque formation, oxidative stress, neuroinflammation and cholinergic neuron damage, decreasing the symptoms typical of AD [96]. In conclusion, by engaging numerous molecular and signaling transduction pathways, allicin may be a candidate molecule for combating neuroinflammation (Figure 4) [88].…”

Section: Allicinmentioning

confidence: 97%

Therapeutic Potential of Allicin and Aged Garlic Extract in Alzheimer’s Disease

Tedeschi

Nigro

Travagli

et al. 2022

IJMS

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Garlic, Allium sativum, has long been utilized for a number of medicinal purposes around the world, and its medical benefits have been well documented. The health benefits of garlic likely arise from a wide variety of components, possibly working synergistically. Garlic and garlic extracts, especially aged garlic extracts (AGEs), are rich in bioactive compounds, with potent anti-inflammatory, antioxidant and neuroprotective activities. In light of these effects, garlic and its components have been examined in experimental models of Alzheimer’s disease (AD), the most common form of dementia without therapy, and a growing health concern in aging societies. With the aim of offering an updated overview, this paper reviews the chemical composition, metabolism and bioavailability of garlic bioactive compounds. In addition, it provides an overview of signaling mechanisms triggered by garlic derivatives, with a focus on allicin and AGE, to improve learning and memory.

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“…These are solid-phase sandwich ELISA read at 450 nm using a microtitre plate reader. The IL-1β, TNF-α, and IL-6 concentrations were determined using standard curves [21,22].…”

Section: Estimation Of Neuroin Ammatory Markers (Tnf-α Il-1β and Il-6)mentioning

confidence: 99%

Effects of Lansoprazole administration on hippocampal cell apoptosis, learning and memory deficits in adult rats via activated of Tau Phosphorylation, Aβ (1–42) Pathway

Aran

Gupta

Singh³

2022

Preprint

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Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by memory loss and dementia, caused by changes in the cortical milieu, such as neuroinflammation, oxidative stress, and accumulation of beta-amyloid (Aβ) in the brain. The drug-induced cognitive impairment is more common in the elderly than in younger people. The research-using valid animal models may help determine the effective and safe medicine for AD treatment. Studies have found that patients who used lansoprazole for long-term therapy for ulcers, Zollinger-Ellison syndrome, and gastroesophageal reflux disease (GERD) who may suffer from memory problems. The novel research was designed to check whether lansoprazole administration to rats may enhance oxidative stress, Aβ accumulation and neurodegeneration. In the current study, rats were given lansoprazole at doses of 15 and 30 mg/kg p.o. for 28 days. The Morris water maze and Probe trial were used to assess rats spatial and recognition memory deficits. On day 29, the rats were sacrificed, and the brain (hippocampus) was used to test for biochemicals (glutathione, superoxide dismutase, catalase, lipid peroxidation, and nitrite), neuroinflammatory markers (IL-1β, TNF-α & IL-6) neurotransmitters (ACh, GABA, and Glutamate), Aβ(1–42) level, nuclear factor-kappa B (NF-κB) analysis, and blood-brain barrier (BBB) disruption activity. Lansoprazole administrated raised inflammatory cytokines release, oxidative stress, altered neurotransmitter concentration, tau protein phosphorylation, and promoted the Aβ accumulation in the brain. These findings showed that lansoprazole treatment for four weeks caused neurobiological alteration in rats and degeneration of the endogenous antioxidant defense system.

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Allicin ameliorates aluminium- and copper-induced cognitive dysfunction in Wistar rats: relevance to neuro-inflammation, neurotransmitters and Aβ(1–42) analysis

Cited by 37 publications

References 44 publications

Neuroprotective efficacy of the bacterial metabolite, prodigiosin, against aluminium chloride‐induced neurochemical alternations associated with Alzheimer's disease murine model: Involvement of Nrf2/HO‐1/NF‐κB signaling

Neuroprotective efficacy of the bacterial metabolite, prodigiosin, against aluminium chloride‐induced neurochemical alternations associated with Alzheimer's disease murine model: Involvement of Nrf2/HO‐1/NF‐κB signaling

Therapeutic Potential of Allicin and Aged Garlic Extract in Alzheimer’s Disease

Effects of Lansoprazole administration on hippocampal cell apoptosis, learning and memory deficits in adult rats via activated of Tau Phosphorylation, Aβ (1–42) Pathway

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