Chronic acarbose treatment alleviates age-related behavioral and biochemical changes in SAMP8 mice

Tong, Jing-Jing; Chen, Guihai; Wang, Fang; Li, Xuewei; Cao, Lei; Xu, Shutu; Tao, Fei; Yan, Wu; Wei, Zhao‐Jun

doi:10.1016/j.bbr.2015.01.052

Cited by 31 publications

(24 citation statements)

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“…Moreover, our data also showed that the increased Syt-1 and decreased Stx-1 were associated with decreased ability in terms of spatial learning and memory in the RAWM. These results were in line with previous reports (Chen et al 2007b;Tong et al 2015;VanGuilder et al 2011). As hypothesized, the LPS treatment dose-dependently accelerated the changes of Syt-1 and Stx-1 in the hippocampus of the older CD-1 mice, suggesting that exposure to LPS during pregnancy could accelerate the age-related changes of Syt-1 and Stx-1.…”

Section: Discussionsupporting

confidence: 93%

“…Specifically, H4 acetylation on the K8 site (H4K8ac) is involved in the formation of long-term memories (Intlekofer et al 2013;McQuown et al 2011). Recently, our studies have also indicated that the oral long-term administration of acarbose or 1-Deoxynojirimycin can alleviate age-related impairments related to spatial learning and memory in SAMP8 mice Tong et al 2015), and the increased H4K8ac may be associated with this alleviation Yan et al 2015).…”

Section: Introductionmentioning

confidence: 85%

“…Our previous and other studies have shown that the hippocampal level of Syt-1 increases with aging and is associated with AAMI in senescence-accelerated prone mice P8 (SAMP8) (Chen et al 2007b;Tong et al 2015), whereas Stx-1 levels decrease in normal-aged rodents VanGuilder et al 2011) and transgenic AD mice (Wirths and Bayer 2010). So, Aβ 42 , p-tau, Syt-1, and Stx-1 can be regarded as age-related neurobiochemical indicators linked to AAMI.…”

Section: Introductionmentioning

confidence: 88%

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Inflammatory insult during pregnancy accelerates age-related behavioral and neurobiochemical changes in CD-1 mice

Wang

Chen

et al. 2016

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Data shows that inflammation during pregnancy significantly exerts a long-term influence on offspring, such as increasing the risk of adult cognition decline in animals. However, it is unclear whether gestational inflammation affects the neurobehavioral and neurobiochemical outcomes in the motherself during aging. In this study, pregnant CD-1 mice intraperitoneally received lipopolysaccharide (LPS) in two doses (25 and 50 g/kg, respectively) or normal saline daily during gestational days 15-17. At the age of 15 months, a battery of behavioral tasks was employed to evaluate their species-typical behaviors, sensorimotor ability, anxiety levels, and spatial learning and memory abilities. An immunohistochemical method was utilized preliminarily to detect neurobiochemical indicators consisting of amyloid-β, p h o s p h o r y l a t e d t a u , p r e s y n a p t i c p r o t e i n s synaptotagmin-1 and syntaxin-1, glial fibrillary acidic protein (GFAP), and histone-4 acetylation on the K8 site (H4K8ac). The behavioral results showed that LPS exposure during pregnancy exacerbated a decline in 15-month-old CD-1 mice's abilities to nest, their sensorimotor and spatial learning and memory capabilities, and increased their anxiety levels. The neurobiochemical results indicated that gestational LPS exposure also intensified age-related hippocampal changes, including increased amyloid-β 42 , phosphorylated tau, synaptotagmin-1 and GFAP, and decreased syntaxin-1 and H4K8ac. Our results suggested that the inflammatory insult during pregnancy could be an important risk factor for the development of Alzheimer's disease, and the H4K8 acetylation might play an important role in the underlying mechanism. This study offers a perspective for improving strategies that support healthy development and successful aging.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 88%

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Inflammatory insult during pregnancy accelerates age-related behavioral and neurobiochemical changes in CD-1 mice

Wang

Chen

et al. 2016

AGE

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“…The age-related behavioral performance is closely related to the serological and histochemical data. These results indicate that the acarbose treatment can alleviate the age-related behavioral deficits and biochemical changes in SAMP8 mice [40] . The research provides the first laboratory evidence that acarbose has the potential in the treatment of cognitive decline and the prevention of brain aging.…”

Section: Alpha-glucosidase Inhibitorsmentioning

confidence: 61%

“…In our recent published research, we use the SAMP8 mice, a model with characteristics of accelerated aging, to explore the effect of long-term treatment with acarbose on the age-related behavioral and biochemical changes [40] . The mice in the acarbose group are administered acarbose by drinking water (20mg/kg/d) from 3 to 9 months of age.…”

Section: Alpha-glucosidase Inhibitorsmentioning

confidence: 99%

Fight against Glucose Rescues Age-Related Cognitive Decline

Tong

Chen

2016

Neurosci Commun

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Aging is commonly associated with dysfunctions of various systems, especially the cognitive decline that seriously diminishes the independence and life quality of old individuals. Exploring the approaches for maintaining a healthy brain is now a critical public health concern. Calorie restriction (CR) has been known to extend longevity, promote metabolic health, and delay the progress of aging and the risk of age-related diseases, such as type 2 diabetes and Alzheimer's disease (AD). Studies have shown that CR improves the insulin sensitivity. Moreover, defected insulin signaling in individuals with or without diabetes is related to a higher risk of age-related cognitive deficits or AD. Evidences suggest that treatment of diabetes mimics the activity of CR, modulating the metabolism of glucose and lipid and the function of insulin system, thus may has the anti-aging potential. In this paper, we reviewed the laboratory experiment and clinical data that focused on the protective role of CR, and that investigated the effect of several types of common agents for diabetes treatment on aging or cognitive ability. The progress in recent years inspires researchers to explore the mechanisms of age-related cognitive decline, and search for safe and effective therapeutic strategies. In the future, more high-quality studies are required to optimize the application of CR or diabetes therapies on the prevention or treatment of brain aging.

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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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Chronic acarbose treatment alleviates age-related behavioral and biochemical changes in SAMP8 mice

Cited by 31 publications

References 83 publications

Inflammatory insult during pregnancy accelerates age-related behavioral and neurobiochemical changes in CD-1 mice

Inflammatory insult during pregnancy accelerates age-related behavioral and neurobiochemical changes in CD-1 mice

Fight against Glucose Rescues Age-Related Cognitive Decline

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

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