Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced Inflammation

Alzheimer’s disease (AD) is a rapidly growing epidemic with a heavy social and economic burden. Evidence suggests that systemic inflammation, dysregulation of the immune response and the resulting neuroinflammation and neurodegeneration play a significant role in AD pathogenesis. Currently, given th...

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Main Authors: Davide Decandia, Francesca Gelfo, Eugenia Landolfo, Francesca Balsamo, Laura Petrosini, Debora Cutuli
Format: Article
Language:English
Published: MDPI AG 2023-03-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/24/6/5921
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author Davide Decandia
Francesca Gelfo
Eugenia Landolfo
Francesca Balsamo
Laura Petrosini
Debora Cutuli
author_facet Davide Decandia
Francesca Gelfo
Eugenia Landolfo
Francesca Balsamo
Laura Petrosini
Debora Cutuli
author_sort Davide Decandia
collection DOAJ
description Alzheimer’s disease (AD) is a rapidly growing epidemic with a heavy social and economic burden. Evidence suggests that systemic inflammation, dysregulation of the immune response and the resulting neuroinflammation and neurodegeneration play a significant role in AD pathogenesis. Currently, given that there is no fully convincing cure for AD, the interest in lifestyle factors (such as diet), which potentially delay onset and reduce the severity of symptoms, is increasing. This review is aimed at summarizing the effects of dietary supplementation on cognitive decline, neuroinflammation and oxidative stress in AD-like animal models with a focus on neuroinflammation induced by lipopolysaccharide (LPS) injection, which mimics systemic inflammation in animals. The compounds reviewed include curcumin, krill oil, chicoric acid, plasmalogens, lycopene, tryptophan-related dipeptides, hesperetin and selenium peptides. Despite the heterogeneity of these compounds, there is a strong consensus on their counteracting action on LPS-induced cognitive deficits and neuroinflammatory responses in rodents by modulating cell-signaling processes, such as the NF-κB pathway. Overall, dietary interventions could represent an important resource to oppose AD due to their influence in neuroprotection and immune regulation.
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spelling doaj.art-218cb3327f3e45cfa362ce2a9a6ce0612023-11-17T11:41:00ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-03-01246592110.3390/ijms24065921Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced InflammationDavide Decandia0Francesca Gelfo1Eugenia Landolfo2Francesca Balsamo3Laura Petrosini4Debora Cutuli5IRCCS Fondazione Santa Lucia, Via Ardeatina 306, 00179 Rome, ItalyIRCCS Fondazione Santa Lucia, Via Ardeatina 306, 00179 Rome, ItalyIRCCS Fondazione Santa Lucia, Via Ardeatina 306, 00179 Rome, ItalyIRCCS Fondazione Santa Lucia, Via Ardeatina 306, 00179 Rome, ItalyIRCCS Fondazione Santa Lucia, Via Ardeatina 306, 00179 Rome, ItalyIRCCS Fondazione Santa Lucia, Via Ardeatina 306, 00179 Rome, ItalyAlzheimer’s disease (AD) is a rapidly growing epidemic with a heavy social and economic burden. Evidence suggests that systemic inflammation, dysregulation of the immune response and the resulting neuroinflammation and neurodegeneration play a significant role in AD pathogenesis. Currently, given that there is no fully convincing cure for AD, the interest in lifestyle factors (such as diet), which potentially delay onset and reduce the severity of symptoms, is increasing. This review is aimed at summarizing the effects of dietary supplementation on cognitive decline, neuroinflammation and oxidative stress in AD-like animal models with a focus on neuroinflammation induced by lipopolysaccharide (LPS) injection, which mimics systemic inflammation in animals. The compounds reviewed include curcumin, krill oil, chicoric acid, plasmalogens, lycopene, tryptophan-related dipeptides, hesperetin and selenium peptides. Despite the heterogeneity of these compounds, there is a strong consensus on their counteracting action on LPS-induced cognitive deficits and neuroinflammatory responses in rodents by modulating cell-signaling processes, such as the NF-κB pathway. Overall, dietary interventions could represent an important resource to oppose AD due to their influence in neuroprotection and immune regulation.https://www.mdpi.com/1422-0067/24/6/5921Alzheimer’s diseasecognitionneuroinflammationoxidative stressneurodegenerationanimal models
spellingShingle Davide Decandia
Francesca Gelfo
Eugenia Landolfo
Francesca Balsamo
Laura Petrosini
Debora Cutuli
Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced Inflammation
International Journal of Molecular Sciences
Alzheimer’s disease
cognition
neuroinflammation
oxidative stress
neurodegeneration
animal models
title Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced Inflammation
title_full Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced Inflammation
title_fullStr Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced Inflammation
title_full_unstemmed Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced Inflammation
title_short Dietary Protection against Cognitive Impairment, Neuroinflammation and Oxidative Stress in Alzheimer’s Disease Animal Models of Lipopolysaccharide-Induced Inflammation
title_sort dietary protection against cognitive impairment neuroinflammation and oxidative stress in alzheimer s disease animal models of lipopolysaccharide induced inflammation
topic Alzheimer’s disease
cognition
neuroinflammation
oxidative stress
neurodegeneration
animal models
url https://www.mdpi.com/1422-0067/24/6/5921
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