Lipopolysaccharide-Induced Spatial Memory and Synaptic Plasticity Impairment Is Preventable by Captopril

Abareshi, Azam; Anaeigoudari, Akbar; Norouzi, Fatemeh; Shafei, Mohammad Naser; Boskabady, Mohammad Hossein; Khazaei, Majid; Hosseini, Mahmoud

doi:10.1155/2016/7676512

Cited by 33 publications

(24 citation statements)

References 42 publications

(58 reference statements)

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“…The short-term spatial memory tested in the Y-maze and long-term object recognition memory tested in NORT are hippocampus-dependent memory types (Cohen et al, 2013; Albani et al, 2014; Pioli et al, 2014). Inflammation in the hippocampus is reported to have impaired these types of memory, and the suppression of inflammation subsequently improved these memory impairments (Miwa et al, 2011; Abareshi et al, 2016). Evidence from these reports together with the findings in our present study suggest that dietary IAA is capable of suppressing microglial inflammatory responses in aged mice, which might be associated with the prevention of the decline in hippocampal memory associated with aging.…”

Section: Discussionmentioning

confidence: 99%

Iso-α-acids, Hop-Derived Bitter Components of Beer, Attenuate Age-Related Inflammation and Cognitive Decline

Ano

Ohya

Kondö

et al. 2019

Front. Aging Neurosci.

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With the aging population rapidly increasing worldwide, preventive measures and treatments for age-related cognitive decline and dementia are of utmost importance. We have previously demonstrated that the consumption of iso-α-acids (IAA), which are hop-derived bitter compounds in beer, prevents the formation of disease pathology in a transgenic mouse model of Alzheimer’s disease (AD). However, the effect of IAA consumption on age-related cognitive decline is unknown. In the present study, we examined the effect of long-term and short-term dietary consumption of IAA, on age-related memory impairments and inflammation in the hippocampus of aged mice. When compared with young mice, aged mice showed impairment in spatial working memory during the Y-maze spontaneous alternation test, impairment in object recognition memory during the novel object recognition test (NORT), a pro-inflammatory hippocampal microglial phenotype with increased CD86 expression and inflammatory cytokine production, increased levels of glutamate and amyloid β1–42, and decreased levels of dopamine (DA). In aged mice fed IAA for 3 months, the age-related alterations in memory, microglial inflammation, and glutamate, amyloid β1–42, and DA levels were all significantly attenuated. Additionally, the oral administration of IAA for 7 days in aged mice with memory impairment, also improved spatial and object recognition memory. These results suggest that IAA consumption prevents inflammation in the hippocampus and ameliorates age-related cognitive decline.

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Section: Discussionmentioning

confidence: 99%

Iso-α-acids, Hop-Derived Bitter Components of Beer, Attenuate Age-Related Inflammation and Cognitive Decline

Ano

Ohya

Kondö

et al. 2019

Front. Aging Neurosci.

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“…The resulting neurocognitive dysfunction has much the same origins as microglial activation induced by PICs but there is some evidence to suggest that the adverse effects on adult neurogenesis, memory deposition and recall, synaptic plasticity and long-term potentiation following elevated systemic LPS is primarily mediated by elevated IL-1β in the hippocampus (Abareshi et al 2016; Li et al 2017; Nolan et al 2005). …”

Section: Consequences Of Chronic Systemic Iandonsmentioning

confidence: 99%

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.

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“…This view has been encompassed in the "fetal origin of adult disease" hypothesis (Benarroch, 2013). Studies have indicated that exposure to inflammation in the embryonic period (Qin et al, 2007;Abareshi et al, 2016) or to stress in adolescence (Speisman et al, 2013;Shields et al, 2017) may be involved in the occurrence of the age-associated learning and memory impairments.…”

Section: Introductionmentioning

confidence: 99%

Effects of Embryonic Inflammation and Adolescent Psychosocial Environment on Cognition and Hippocampal Staufen in Middle-Aged Mice

Zhang

et al. 2020

Front. Aging Neurosci.

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Accumulating evidence has indicated that embryonic inflammation could accelerate age-associated cognitive impairment, which can be attributed to dysregulation of synaptic plasticity-associated proteins, such as RNA-binding proteins (RBPs). Staufen is a double-stranded RBP that plays a critical role in the modulation of synaptic plasticity and memory. However, relatively few studies have investigated how embryonic inflammation affects cognition and neurobiology during aging, or how the adolescent psychosocial environment affects inflammation-induced remote cognitive impairment. Consequently, the aim of this study was to investigate whether these adverse factors can induce changes in Staufen expression, and whether these changes are correlated with cognitive impairment. In our study, CD-1 mice were administered lipopolysaccharides (LPS, 50 µg/kg) or an equal amount of saline (control) intraperitoneally during days 15-17 of gestation. At 2 months of age, male offspring were randomly exposed to stress (S), an enriched environment (E), or not treated (CON) and then assigned to five groups: LPS, LPS+S, LPS+E, CON, and CON+S. Mice were evaluated at 3-month-old (young) and 15-month-old (middle-aged). Cognitive function was assessed using the Morris water maze test, while Staufen expression was examined at both the protein and mRNA level using immunohistochemistry/western blotting and RNAscope technology, respectively. The results showed that the middle-aged mice had worse cognitive performance and higher Staufen expression than young mice. Embryonic inflammation induced cognitive impairment and increased Staufen expression in the middle-aged mice, whereas adolescent stress/an enriched environment would accelerated/mitigated these effects. Meanwhile, Staufen expression was closely correlated with cognitive performance. Our findings suggested embryonic inflammation can accelerate age-associated learning and memory impairments, and these effects may be related to the Staufen expression.

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Lipopolysaccharide-Induced Spatial Memory and Synaptic Plasticity Impairment Is Preventable by Captopril

Cited by 33 publications

References 42 publications

Iso-α-acids, Hop-Derived Bitter Components of Beer, Attenuate Age-Related Inflammation and Cognitive Decline

Iso-α-acids, Hop-Derived Bitter Components of Beer, Attenuate Age-Related Inflammation and Cognitive Decline

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Effects of Embryonic Inflammation and Adolescent Psychosocial Environment on Cognition and Hippocampal Staufen in Middle-Aged Mice

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