Age‐related loss of synapses in the frontal cortex of SAMP10 mouse: A model of cerebral degeneration

Shimada, Atsuyoshi; Keino, Hiromi; Satoh, Mamoru; Kishikawa, Masao; Hosokawa, Masanori

doi:10.1002/syn.10209

Cited by 56 publications

(36 citation statements)

References 33 publications

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“…[39][40][41] In aged SAMP10, a decreased level of synaptophysin, a presynaptic vesicular protein, and synaptic loss have been observed in the atrophied anterior cerebral cortex, 21) and cognitive performance has been found to be associated with alterations in cerebral atrophy 24,42) and the level of synaptophysin. 23) In mice that ingested b-CRX, however, the wet weight of the cerebrum did not change significantly and an increase of synaptophysin was observed but it was not significant (data not shown).…”

Section: Discussionmentioning

confidence: 99%

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Beta-Cryptoxanthin, Plentiful in Japanese Mandarin Orange, Prevents Age-Related Cognitive Dysfunction and Oxidative Damage in Senescence-Accelerated Mouse Brain

Unno

Sugiura

Ogawa

et al. 2011

Biological & Pharmaceutical Bulletin

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The brain is highly susceptible to oxidative damage because it consumes a large amount of oxygen and generates many free radicals as normal products of cellular metabolism. [1][2][3] In addition, the brain contains diverse lipid components and fewer antioxidant enzymes than other organs. 4) Although the antioxidant defense system responds to an increase in the production of reactive oxygen species (ROS) or peroxide under normal conditions, it gives rise to oxidative stress in the brain if an imbalance occurs between the production of ROS and the cellular defense capability. Aging is an important risk factor of this imbalance. Accumulation of oxidative damage is the most probable cause of the decline in learning and memory with aging.5) Preventing the accumulation of ROS-causing oxidative damage might suppress cognitive dysfunction.Several studies have demonstrated that dietary antioxidants from fruits and vegetables prevent oxidative stress in the brain.6-10) Neuroprotective dietary compounds have an essential role in reducing aging of the brain.11,12) Beta-cryptoxanthin (b-CRX, (3R)-b,b-caroten-3-ol, Fig. 1) is the main precursor of vitamin A in citrus juices.13) This carotenoid is not fully cleaved in vitamin A in the gut and it is therefore recovered in human plasma.14) Recent clinical studies indicated that the frequent intake of citrus fruits increases plasma b-CRX concentrations and reported b-CRX to be a biomarker of mandarin consumption.15) The concentrations of carotenoids, tocopherols and retinols were investigated in an aged human brain.16) An age-related decline in retinol, total tocopherols, total xanthophylls (oxygenated carotenoids) and total carotenoids was observed in frontal but not in occipital lobes. The antioxidative activity of b-CRX has been reported to scavenge radicals, 17) and to suppress lipid peroxidation 18) and nitrogen oxide production.19) The important role of antioxidants in the brain is thus expected. In this study, we investigated the effect of consumption of b-CRX (Fig. 1) and Satsuma mandarin orange (mandarin, Citrus unshiu MARC.) juice on brain function because b-CRX is rich in mandarin, the most popular fruit in Japan.We investigated the effect of b-CRX and mandarin juice on the brain using senescence-prone mouse strain 10 (SAMP10), which is a useful model of brain aging with a short life span and declined learning ability in later life. 20,21) Moreover, the production of superoxide anion was higher in SAMP10 than in other mice with normal longevity and brain function. 22) In addition, our previous data indicates that the consumption of green tea catechin (catechin), a potent antioxidant in green tea, suppressed brain dysfunction and DNA oxidative damage in aged SAMP10. [23][24][25] These data strongly suggest that chronic intake of other antioxidants in fruits and vegetables also play a role in reducing the risk of age-related brain dysfunction. In this study, we investigated the effect of chronic consumption of b-CRX and mandarin juice, which contains a similar amount of ...

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Section: Discussionmentioning

confidence: 99%

“…20,21) Moreover, the production of superoxide anion was higher in SAMP10 than in other mice with normal longevity and brain function. 22) In addition, our previous data indicates that the consumption of green tea catechin (catechin), a potent antioxidant in green tea, suppressed brain dysfunction and DNA oxidative damage in aged SAMP10.…”

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confidence: 94%

Beta-Cryptoxanthin, Plentiful in Japanese Mandarin Orange, Prevents Age-Related Cognitive Dysfunction and Oxidative Damage in Senescence-Accelerated Mouse Brain

Unno

Sugiura

Ogawa

et al. 2011

Biological & Pharmaceutical Bulletin

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“…The SAMP8 tend to have more accelerated impairments of learning and memory, and the deficits are more pronounced than the SAMP10 (Miyamoto 1997). Furthermore, previous research has highlighted the age-related hippocampal changes in the SAMP8, whereas much of the focus of research in the SAMP10 has been on neocortical changes, although this distinction is not absolute (Flood and Morley 1998;Han et al 2004;Sano et al 2004;Shimada 1999;Shimada et al 2003). Because we were interested in the possible relationship between circadian rhythm disruptions and hippocampal learning and memory deficits, we used the SAMP8 rather than the SAMP10 for our studies.…”

Section: Senescence-accelerated Mouse As a Model Of Agingmentioning

confidence: 99%

Age-related disruptions of circadian rhythm and memory in the senescence-accelerated mouse (SAMP8)

Pang

Miller

Fortress

et al. 2006

AGE

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Common complaints of the elderly involve impaired cognitive abilities, such as loss of memory and inability to attend. Although much research has been devoted to these cognitive impairments, other factors such as disrupted sleep patterns and increased daytime drowsiness may contribute indirectly to impaired cognitive abilities. Disrupted sleep-wake cycles may be the result of age-related changes to the internal (circadian) clock. In this article, we review recent research on aging and circadian rhythms with a focus on the senescence-accelerated mouse (SAM) as a model of aging. We explore some of the neurobiological mechanisms that appear to be responsible for our aging clock, and consider implications of this work for age-related changes in cognition.Key words aging . C-Fos . circadian rhythms . mouse . running wheel . SAMP8 . suprachiasmatic nucleus Cognitive impairments are well-known complaints of the elderly. Despite their obvious clinical importance, many questions remain unanswered. One important issue concerns whether cognitive impairments are due to direct alterations in the cognitive function, or to other difficulties that may in turn result in cognitive deficits. For example, the elderly often report poor night-time sleep quality, daytime sleepiness, lack of energy, and difficulty adjusting to a time shift (increased "jet lag"). Could these effects contribute to cognitive impairments?Although a confluence of factors may lead to poor sleep quality, etc., it is likely that one general culprit is aging of the internal (circadian) clock that regulates these behaviors (Munch et al. 2005;Turek et al. 1995;Weitzman et al. 1982). Moreover, evidence suggests that our internal clock may also mediate cognitive functioning (Antoniadis et al. 2000;Brock 1991, Stone 1989van Gool 1986;van Someren et al. 1993a). In this article, we review recent research on aging and circadian rhythms, with a focus on the senescence-accelerated mouse line. We explore some of the neurobiological mechanisms that appear to be responsible for our aging clock, and consider implications of this work for the study of age-related changes in cognition.Circadian rhythms are predictable and regularly occurring daily changes in behavior and physiological states. The term circadian, literally meaning "around a day," has its origins in two Latin words: Circa (around) and dies (day). Two defining characteristics AGE (2006) of circadian rhythms are their continued persistence in the absence of external cues in the environment and their ability to be entrained (synchronized) by environmental cues. With respect to the former property, it is the endogenous (self-sustaining) nature of circadian rhythms that engenders an internal clock. With respect to the latter property, the major external cue that serves to synchronize the circadian rhythms of humans and other mammals is light, but almost any periodic event can act as a Zeitgeber ("time-giver").Research on the biological basis of circadian rhythms in humans and other mammals implicates the s...

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“…In addition, we recently reported that the ingestion of GSE ameliorated cognitive dysfunction and amyloid β (Aβ) accumulation in aged senescence-accelerated mice (SAMP10) [10]. SAMP10 mice exhibit a short life span, brain atrophy in the frontal region, neuronal loss and cognitive dysfunction with aging [11][12][13]. The expression of Ptgds, which encodes lipocalin-type prostaglandin D2 synthase, a putative endogenous Αβ-chaperone, was significantly associated with a green soybean diet [10,14].…”

Section: Introductionmentioning

confidence: 99%

Improvement in Cognitive Function with Green Soybean Extract May Be Caused by Increased Neuritogenesis and BDNF Expression

Minami¹,

Nakayama²,

Kimura³

et al. 2017

J Food Process Technol

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Green soybean (Glycine max L.), which was used in this study, retains the green color of the seed coat cotyledon even after ripening, even though many soybean cultivars become yellow during maturation. We have reported that ingestion of green soybean extract (GSE) suppressed cognitive dysfunction and reduced amyloid β accumulation more than yellow soybean extract (YSE) in aged senescence-accelerated (SAMP10) mice, a mouse model of brain senescence. To clarify the mechanism by which GSE suppresses cognitive dysfunction, we examined the effect of GSE and YSE on neurite outgrowth in human neuroblastoma SHSY-5Y cells. GSE significantly increased cell number and neurite outgrowth at 5 ng/ml (as isoflavones, 30 pg/ml), but the effect of YSE was lower than that of GSE. Although isoflavone aglycones, genistein and daidzein increased the number of SH-SY5Y cells, the effect was only observed at a high concentration [0.05 µM (13 ng/ml)]. ICR mice were fed a diet containing 3% soybean extract for 3 weeks (3-4 g/kg; as isoflavones, ca. 20 mg/kg) to examine cognitive function. Learning and memory abilities, as evaluated by a step-through passive avoidance task, a Y-maze and a novel object recognition test, were significantly higher in mice that ingested GSE than control mice that were fed a normal diet. The expression of brain-derived neurotrophic factor (BDNF) in the hippocampus, as detected by western blot analysis, was higher in mice that ingested GSE than in control mice. This study suggests that the ingestion of GSE enhances learning and memory abilities in mice. The effect by which GSE improved cognitive function appears to be caused, in part, by increased neuritogenesis and BDNF expression. In the present study, in order to clarify the mechanism by which GSE suppresses brain aging, we first examined the effects of GSE and yellow soybean extract (YSE) on SH-SY5Y cells, which have been used to observe neurotrophic activity-inducing neurite outgrowth as well as cell number growth in cell culture system [18,19]. This activity was compared with that of soy isoflavones such as genistein and daidzein. We also examined whether a relatively short period of administration of GSE could alter learning and memory abilities of young mice using a Y-maze, novel-object recognition and a step-through passive avoidance task. In addition, since brain-derived neurotrophic factor (BDNF) is a key mediator involved in both neurogenesis and cognitive function, we examined the expression of BDNF in the hippocampus of mice that ingested GSE. Improvement in Cognitive Function Materials and Methods Preparation of soybean extractJapanese cultivars of green soybean ('Echigomidori') and yellow soybean ('Fukuyutaka') were used. Soybeans (10 g) crushed into a

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Age‐related loss of synapses in the frontal cortex of SAMP10 mouse: A model of cerebral degeneration

Cited by 56 publications

References 33 publications

Beta-Cryptoxanthin, Plentiful in Japanese Mandarin Orange, Prevents Age-Related Cognitive Dysfunction and Oxidative Damage in Senescence-Accelerated Mouse Brain

Beta-Cryptoxanthin, Plentiful in Japanese Mandarin Orange, Prevents Age-Related Cognitive Dysfunction and Oxidative Damage in Senescence-Accelerated Mouse Brain

Age-related disruptions of circadian rhythm and memory in the senescence-accelerated mouse (SAMP8)

Improvement in Cognitive Function with Green Soybean Extract May Be Caused by Increased Neuritogenesis and BDNF Expression

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