Investigation of the optimal dose for experimental lipopolysaccharide-induced recognition memory impairment: behavioral and histological studies

Alzahrani, Noor Ahmed; Bahaidrah, Khulud Abdullah; Mansouri, Rasha A.; Alsufiani, Hadeil M.; Alghamdi, Badrah S.

doi:10.31083/j.jin2102049

Cited by 14 publications

(16 citation statements)

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“…Recently, Alzahrani and colleagues directly addressed the problem of LPS dosage in the chronic intraperitoneal administration model of memory impairment [ 14 ]. Based on previous publications in this field, they investigated the influence of 7 days treatment with 250, 500 and 750 μg/kg LPS on recognition memory impairment in mice.…”

Section: Technical Aspects Of Lps Model Execution—focus On Ad and Pd ...mentioning

confidence: 99%

“…Neuroinflammation has been associated with several neurological diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis, multiple sclerosis, Huntington’s disease, and brain cancer [ 1 , 2 , 4 , 9 , 14 ]. These neurodegenerative diseases and their complications are a grave concern for public health given their incurability, reduction in patient’s quality of life and self-independence, and the increasing number of cases every year [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

“…To model the complexity of processes involved in the neuroinflammation and their outcomes, e.g., cognitive dysfunction, in vivo studies are intensively utilized. For this purpose, LPS is used as one of the most potent pro-inflammatory stimuli [ 14 , 28 ].…”

Section: Introductionmentioning

confidence: 99%

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Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

Skrzypczak-Wiercioch

Sałat

2022

Molecules

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Despite advances in antimicrobial and anti-inflammatory therapies, inflammation and its consequences still remain a significant problem in medicine. Acute inflammatory responses are responsible for directly life-threating conditions such as septic shock; on the other hand, chronic inflammation can cause degeneration of body tissues leading to severe impairment of their function. Neuroinflammation is defined as an inflammatory response in the central nervous system involving microglia, astrocytes, and cytokines including chemokines. It is considered an important cause of neurodegerative diseases, such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Lipopolysaccharide (LPS) is a strong immunogenic particle present in the outer membrane of Gram-negative bacteria. It is a major triggering factor for the inflammatory cascade in response to a Gram-negative bacteria infection. The use of LPS as a strong pro-inflammatory agent is a well-known model of inflammation applied in both in vivo and in vitro studies. This review offers a summary of the pathogenesis associated with LPS exposure, especially in the field of neuroinflammation. Moreover, we analyzed different in vivo LPS models utilized in the area of neuroscience. This paper presents recent knowledge and is focused on new insights in the LPS experimental model.

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Section: Technical Aspects Of Lps Model Execution—focus On Ad and Pd ...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

Skrzypczak-Wiercioch

Sałat

2022

Molecules

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“…In the same way, LPS-treated mice displayed a below normal discrimination between familiar and novel objects in the NORT when compared with the normal control group. However, diosmin administration seemed to reinforce the mental capabilities of the LPS-treated mice thereby boosting their memory and cognition in both tests (Alzahrani et al, 2022;Lee et al, 2020). These behavioural alterations are believed to involve such in ammatory mediators as were evaluated in this study.…”

Section: Discussionmentioning

confidence: 52%

Diosmin inhibits neuroinflammation and improves cognitive deficit in lipopolysaccharide-mouse model of Alzheimer’s disease

ADEOLUWA,

ADENIYI,

ADEOLUWA

et al. 2024

Preprint

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Background: Neuroinflammation has been linked to some central alterations such as cognitive and memory impairment which are prominent features of many neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease etc. This study explored the cognitive-enhancing properties of a flavonoid, diosmin, on lipopolysaccharide-induced cognitive impairment in mice. Methodology: Twenty-eight mice were divided into four groups. These groups were scheduled to receive either vehicle or any of the two doses of diosmin. Groups 2-4 were treated with lipopolysaccharide (LPS; 250 µg/kg, i.p.) daily for seven days. Afterwards, all mice were subjected to the Y-maze test and the novel object recognition test (NORT) to assess their spatial and non-spatial working memory, respectively. Subsequently, the mice were sacrificed and brain samples were harvested for biochemical analysis. The data was analysed using one way analysis of variance (ANOVA) and a post hoc test. The level of significance was set at p<0.05. Results: Our data shows that diosmin significantly reversed the LPS-induced neuroinflammation by reducing proinflammatory mediators in the brain and subsequently improving mice memory. Conclusion: Diosmin possesses properties that could be beneficial in symptom management in such inflammation-related disorders.

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“…LPS administration elongates the primary cilium in astrocytes in the brain. It has been reported that inflammation model mice exhibit a decline in cognitive function (33)(34)(35). Therefore, we investigated mouse cognitive function using the novel object recognition (NOR) test for evaluating long-term memory, the open field (OF) test for determining locomotor activity, and the Y-maze test for assessing short-term memory (Fig 2C).…”

Section: Inflammation Model Mice Exhibit An Increase In A1 Astrocyte ...mentioning

confidence: 99%

Astrocyte-specific inhibition of primary cilium functions improves cognitive impairment during neuroinflammation by suppressing A1 astrocyte differentiation

Muhamad,

Furukawa,

Yuri

et al. 2023

Preprint

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A1 astrocytes play a neurotoxic role in various neurodegenerative diseases. While inhibiting the differentiation of A1 astrocytes can slow disease progression, the mechanisms controlling A1 astrocyte differentiation are largely unknown. The primary cilium is a cellular organelle that receives extracellular signals and regulates cell proliferation, differentiation, and maturation. To elucidate the physiological function of the primary cilium in A1 astrocytes, we utilized primary astrocytes and an inflammation mouse model. We found that the length of the primary cilium was increased in astrocytes, and the inhibition of primary cilium formation inhibited their differentiation into A1 astrocytes. Since mice with systemic ciliogenesis defects exhibit embryonic lethality, the function of the primary cilium in adults has remained largely unclear. Therefore, we established conditional knockout (cKO) mice that specifically inhibit primary cilium function in astrocytes upon drug stimulation. In a neuroinflammation mouse model in which lipopolysaccharide (LPS) was intraperitoneally injected into wild-type mice, increases in A1 astrocyte number and primary cilium length were observed in the brain. In contrast, cKO mice exhibited a reduction in the proportions of A1 astrocytes and apoptotic cells in the brain. Additionally, the novel object recognition (NOR) score observed in the cKO mice was higher than that observed in the neuroinflammation model mice. These results suggest that the primary cilium in astrocytes is essential for A1 astrocyte differentiation, which leads to a decline brain function. We propose that regulating astrocyte-specific primary cilium signalling may be a novel strategy for the suppression of neuroinflammation.

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Investigation of the optimal dose for experimental lipopolysaccharide-induced recognition memory impairment: behavioral and histological studies

Cited by 14 publications

References 0 publications

Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

Diosmin inhibits neuroinflammation and improves cognitive deficit in lipopolysaccharide-mouse model of Alzheimer’s disease

Astrocyte-specific inhibition of primary cilium functions improves cognitive impairment during neuroinflammation by suppressing A1 astrocyte differentiation

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