Maternal inflammation linearly exacerbates offspring age-related changes of spatial learning and memory, and neurobiology until senectitude

Li, Xuewei; Cao, Lei; Wang, Fang; Yang, Qian; Tong, Jing-Jing; Li, Xueyan; Chen, Guihai

doi:10.1016/j.bbr.2016.03.011

Cited by 20 publications

(41 citation statements)

References 60 publications

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“…The behavioral experiments including nesting, open field, beam walking, elevated plus maze, OLR, and RAWM were conducted according to our previous studies (Chen et al, ; Li, Cao, et al, ; Li, Wang, et al, ; Tong et al, ).…”

Section: Methodsmentioning

confidence: 99%

“…The strept–avidin–biotin–peroxidase complex (SABC) method was performed as described in our previous studies (Li, Cao, et al, ; Li, Wang, et al, ; Tong et al, ). The main difference is that primary antibodies including rabbit monoclonal anti‐Aβ 42 (1:300) and polyclonal anti‐p‐tauser404 (1:500) and GFAP (1:500) were purchased from the Abcam and Dako.…”

Section: Methodsmentioning

confidence: 99%

“…Besides behavioral and cognitive dysfunctions, maternal infection insult by LPS can lead to certain changes in hippocampal morphology and neurochemistry in offspring, such as neuron loss, altered synaptic transmission, reduced hippocampal neurogenesis, decreased expression of synaptophysin, and increased expression of GFAP in the hippocampal CA1 region (Boksa, ; Graciarena, Depino, & Pitossi, ; Hao et al, ; Lowe, Luheshi, & Williams, ). A recent investigation by our group showed that maternal inflammatory insult by LPS administration during pregnancy worsened the age‐related hippocampal neurobiological indicators (decreased H4K8ac, H3K9ac, and Stx‐1 and increased Syt‐1) in the offspring of CD‐1 mice from midlife (12 months old) to the twilight years (22 months old; Li, Cao, et al, ; Li, Wang, et al, ). However, these previous studies did not comprehensively assess cognitive and behavioral functions in these mice suffered with LPS during late embryogenesis at different age especially old age, nor did they detect AD‐related pathophysiology in the hippocampus.…”

Section: Introductionmentioning

confidence: 92%

“…with LPS 0.79 mg/kg at gestational days (gd) 8, 10, and 12 showed distinct learning and memory decline in their offspring at the ages of 10 and 20 months but not 3 months (Hao, Hao, Li, & Li, ). Our previous studies indicated that pregnant CD‐1 mice intraperitoneally received 50 μg/kg LPS during gd 15–17 accelerated age‐related learning and memory impairment and species‐typical behaviors in middle‐aged offspring (Chen et al, ; Li, Cao, et al, ; Li, Wang, et al, ). Moreover, this LPS effect on learning and memory deficit was also observed in old‐aged offspring mice and thus was even a lower‐dose injection of LPS (25 μg/kg; Li, Cao, et al, ; Li, Wang, et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer‐like behavioral and neuropathological changes in CD‐1 mice

et al. 2020

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Introduction Infections could contribute to Alzheimer's disease (AD) neuropathology in human. However, experimental evidence for a causal relationship between infections during the prenatal phase and the onset of AD is lacking. Methods CD‐1 mothers were intraperitoneally received lipopolysaccharide (LPS) with two doses (25 and 50 μg/kg) or normal saline every day during gestational days 15–17. A battery of behavioral tasks was used to assess the species‐typical behavior, sensorimotor capacity, anxiety, locomotor activity, recognition memory, and spatial learning and memory in 1‐, 6‐, 12‐, 18‐, and 22‐month‐old offspring mice. An immunohistochemical technology was performed to detect neuropathological indicators consisting of amyloid‐β (Aβ), phosphorylated tau (p‐tau), and glial fibrillary acidic protein (GFAP) in the hippocampus. Results Compared to the same‐aged controls, LPS‐treated offspring had similar behavioral abilities and the levels of Aβ42, p‐tau, and GFAP at 1 and 6 months old. From 12 months onward, LPS‐treated offspring gradually showed decreased species‐typical behavior, sensorimotor ability, locomotor activity, recognition memory, and spatial learning and memory, and increased anxieties and the levels of Aβ42, p‐tau, and GFAP relative to the same‐aged controls. Moreover, this damage effect (especially cognitive decline) persistently progressed onwards. The changes in these neuropathological indicators significantly correlated with impaired spatial learning and memory. Conclusions Prenatal exposure to low doses of LPS caused AD‐related features including behavioral and neuropathological changes from midlife to senectitude.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer‐like behavioral and neuropathological changes in CD‐1 mice

et al. 2020

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“…Thus, plasmalogens are important for neurotransmission (117–119). The hippocampus is uniquely sensitive to an age-related decline in function, with reports of short-term memory loss as a consequence of normal aging (120–124). These hippocampal-mediated effects are even more profound in patients with various forms of cognitive impairment, and the hippocampal pathologies of Alzheimer’s disease have been a significant focus in the field for the last several decades.…”

Section: Discussionmentioning

confidence: 99%

Regional changes in CNS and retinal glycerophospholipid profiles with age: a molecular blueprint

Hopiavuori

Agbaga

Brush

et al. 2017

Journal of Lipid Research

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We present here a quantitative molecular blueprint of the three major glycerophospholipid (GPL) classes, phosphatidylcholine (PC), phosphatidylserine (PS), and phosphatidylethanolamine (PE), in retina and six regions of the brain in C57Bl6 mice at 2, 10, and 26 months of age. We found an age-related increase in molecular species containing saturated and monoenoic FAs and an overall decrease in the longer-chain PUFA molecular species across brain regions, with loss of DHA-containing molecular species as the most consistent and dramatic finding. Although we found very-long-chain PUFAs (VLC-PUFAs) (⩾C28) in PC in the retina, no detectable levels were found in any brain region at any of the ages examined. All brain regions (except hippocampus and retina) showed a significant increase with age in PE plasmalogens. All three retina GPLs had di-PUFA molecular species (predominantly 44:12), which were most abundant in PS (∼30%). In contrast, low levels of di-PUFA GPL (1–2%) were found in all regions of the brain. This study provides a regional and age-related assessment of the brain’s lipidome with a level of detail, inclusion, and quantification that has not heretofore been published.

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Accelerated reduction of serum thyroxine and hippocampal histone acetylation links to exacerbation of spatial memory impairment in aged CD-1 mice pubertally exposed to bisphenol-a

Jiang

Cao

Wang

et al. 2016

AGE

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Age-related cognitive decline has been associated with changes in endogenous hormones and epigenetic modification of chromatin, including histone acetylation. Developmental exposure to endocrine disrupting chemicals, such as bisphenol-A (BPA) that produces endocrine disruption and epigenetic changes, may be a risk factor for accelerating cognitive deficits during aging. Thus, we exposed CD-1 mice to BPA (0, 1, and 100 mg/l BPA in the drinking water) orally during puberty (from postnatal days 28 to 56) and investigated whether pubertal BPA exposure exacerbates the age-related impairment of spatial cognition in old age (18 months old) and whether serum sex and thyroid hormones or hippocampal histone acetylation (H3K9ac and H4K8ac) are associated with cognitive effects. A young control group (6 months old) was added to analyze the age effect. Results showed untreated aged mice had marked decline of spatial learning and memory in the novel location recognition and radial six-arm water maze tasks, with decreased levels of these hormones and hippocampal H3K9ac and H4K8ac compared to young controls. The BPA treatment exacerbated age-related spatial cognitive impairment and accelerated the reduction of free thyroxine (FT4), H3K9ac, and H4K8ac, and the 100 mg/l BPA group showed more significant impact. Additionally, correlation analyses revealed that lower levels of FT4, H3K9ac, and H4K8ac were accompanied by decreased spatial memory abilities. We concluded that accelerated reduction of serum FT4 and hippocampal H3K9ac and H4K8ac might be linked to exacerbation of age-related spatial cognitive impairment due to pubertal BPA exposure.

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Maternal inflammation linearly exacerbates offspring age-related changes of spatial learning and memory, and neurobiology until senectitude

Cited by 20 publications

References 60 publications

Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer‐like behavioral and neuropathological changes in CD‐1 mice

Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer‐like behavioral and neuropathological changes in CD‐1 mice

Regional changes in CNS and retinal glycerophospholipid profiles with age: a molecular blueprint

Accelerated reduction of serum thyroxine and hippocampal histone acetylation links to exacerbation of spatial memory impairment in aged CD-1 mice pubertally exposed to bisphenol-a

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