Appearance of amyloid β-like substances and delayed-type apoptosis in rat hippocampus CA1 region through aging and oxidative stress

Fukui, Koji; Takatsu, Hirokatsu; Senoo, Tadashi; Suzuki, Sadao; Abe, Kouichi; Urano, Shiro

doi:10.3233/jad-2005-8309

Cited by 75 publications

(60 citation statements)

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“…Although interestingly, the observations obtained in this study are consistent with the time of appearance of neuronal cell death and amyloid-β in the rat brain caused by oxidative stress [21], whether or not this is correlated with neurodegeneration and the deficit in cognition needs further investigation.…”

Section: Discussionsupporting

confidence: 68%

“…ROS generated by chronic oxidative stress which is experienced over a long period may attack the brain, leading to aging and neurodegeneration [20]. In fact, young rats subjected to hyperoxia as oxidative stress and normal aged rats show an increase in the amount of denatured lipids at nerve terminals that is, TBARS and conjugated diene [2], accumulation of amyloid β in the hippocampus, and neuron apoptosis, resulting in deficit in cognition [9,21]. Thus, reactive products of lipid peroxidation have been considered for long time to be a causal factor of neurodegenerative diseases.…”

Section: Discussionmentioning

confidence: 99%

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Increased F2-Isoprostane Levels in the Rat Brain and Plasma Caused by Oxidative Stress and Aging, and Inhibitory Effect of Vitamin E

Nishio

Miyadera

Sakai

et al. 2006

J. Clin. Biochem. Nutr.

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Summary To determine whether lipid peroxidation induced by reactive oxygen species (ROS) is a causal factor of neurodegeneration during brain aging, we investigated whether F2-isoprostanes, non-cyclooxygenase-derived prostanoids, are formed in the rat brain and plasma by hyperoxia as oxidative stress, and whether their formation is associated with vitamin E status in vivo in association with changes that occur during brain aging. Young rats subjected to hyperoxia for 48 h revealed a marked increase in the levels of F2-isoprostanes in the brain, but not in plasma. A similar increase in F2-isoprostane level was observed in aged rats kept in normal atmosphere. Vitamin E supplementation to young rats markedly inhibited F2-isoprostane formation even after hyperoxia. In contrast, vitamin E-deficient young rats kept in normal atmosphere showed a significant increase in F2-isoprostane level in the brain. These findings indicate that F2-isoprostane formation in the brain has important implications in the etiology of neurodegenerative diseases including Alzheimer's disease during aging, and that the analysis of F2-isoprostane level in plasma does not always reflect neuronal damage cause by oxidative stress. Vitamin E may protect neuronal damage in the brain caused by oxidative stress experienced for a long period during aging.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Increased F2-Isoprostane Levels in the Rat Brain and Plasma Caused by Oxidative Stress and Aging, and Inhibitory Effect of Vitamin E

Nishio

Miyadera

Sakai

et al. 2006

J. Clin. Biochem. Nutr.

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“…In this study, we found axonal degeneration in the hippocampal region of vitamin E-deficient and normal old mice. Previously, we found b-amyloid-like substances in the hippocampal CA1 region of vitamin E-deficient and normal old rats (12). It is possible that axonal degeneration occurs in hippocampal neurons at an early stage in AD patients.…”

Section: Axonal Degeneration In the Hippocampal Ca1 Region Of Vitaminmentioning

confidence: 99%

“…In a previous study, we demonstrated that vitamin E-deficient rats exhibited cognitive dysfunction in several maze tasks (10,11). We have been studying the mechanisms of cognitive dysfunction in this animal model, and have found evidence of apoptosis and b-amyloid-like proteins in the hipocampal CA1 region (12), indicating that cognitive dysfunction in vitamin E-deficient animals may be connected with injury to hippocampal neurons. However, by the time that these signs of neuronal injury are evident, it is difficult to recover cognitive function, because the neurons are severely damaged or have died.…”

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confidence: 99%

Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Fukui

Kawakami

Honjo

et al. 2012

J Nutr Sci Vitaminol

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SummarySeveral lines of evidence demonstrate the relationship between vitamin E deficiency and cognitive dysfunction in rodent models, but little is known about the underlying mechanisms. In this study, we found axonal injury in the hippocampal CA1 region of vitamin E-deficient and normal old mice using immunohistochemical assay. The number of cells in the hippocampal CA1 region of vitamin E-deficient mice and normal old mice was significantly lower than in normal young mice. It is well known that collapsin response mediator protein (CRMP)-2 plays a crucial role in the maintenance of axonal conditions. The expressions of CRMP-2 in the cerebral cortex and hippocampus of vitamin E-deficient mice were significantly lower than both the regions of normal ones. In normal old mice, the expression of CRMP-2 in the cerebral cortex was significantly lower than in the normal ones. In addition, the appearance of microtubule-associated protein (MAP)-light chain 3 (LC3), a major index of autophagy, was higher in the cerebral cortex and hippocampus of vitamin E-deficient mice than in normal young and old mice. These results indicate that axonal degeneration is induced in living tissues, but not cultured cells, and that changes in CRMP-2 and MAP-LC3 may underlie vitamin E-deficiency-related axonal degeneration.

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“…it is well established that aβ possesses neurotoxic activity, which has been associated with peptide self-aggregation and leads to the formation of amyloid-like fibrils, and eventually to neuronal death through apoptosis. Several studies suggest that oxidative stress is involved in an apoptotic mechanism by which excessive roS production leads to neuronal apoptosis in neurodegenerative disorders, such as aβ-induced neuronal apoptosis (5)(6)(7). aβ [25][26][27][28][29][30][31][32][33][34][35] is a short aβ fragment that exhibits large β-sheet fibrils and retains the same neurotoxicity as the full-length peptide (8).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 protects PC12 cells against β-amyloid-induced cell injury

Xie

Wang²,

Li³

et al. 2010

Mol Med Rep

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Abstract. excessive accumulation of β-amyloid (aβ) has been proposed as a pivotal event in the pathogenesis of alzheimer's disease. Possible mechanisms underlying aβ-induced neuronal cytotoxicity include oxidative stress and apoptosis. reactive oxygen species (roS) have been proposed to be involved in the apoptotic mechanism of aβ-induced cytotoxicity. Ginsenoside rb1 (Grb1), which is among the key compounds of ginsenoside, found in ginseng, may be a potent scavenger of roS. To examine the potential protective effect of Grb1 in aβ 25-35 -induced cytotoxicity, cells were pre-treated with Grb1 for 24 h, and then aβ [25][26][27][28][29][30][31][32][33][34][35] was added to the medium for an additional 24 h. exposure to aβ led to the accumulation of roS and lipid peroxidation, eventually causing a decrease in the Bcl-2/ Bax ratio, caspase-3 activation, cell apoptosis and cell death. Pre-treatment with Grb1 not only inhibited aβ-induced roS overproduction and lipid peroxidation, but also increased the Bcl-2/Bax ratio and attenuated caspase-3 activation, thereby improving cell survival. Grb1 may therefore act as a roS scavenger, and such antioxidant properties may play a protective role against aβ-induced cell injury. Further exploration of Grb1 antioxidant properties may provide novel therapeutic strategies for the treatment of alzheimer's disease.

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Appearance of amyloid β-like substances and delayed-type apoptosis in rat hippocampus CA1 region through aging and oxidative stress

Cited by 75 publications

References 0 publications

Increased F2-Isoprostane Levels in the Rat Brain and Plasma Caused by Oxidative Stress and Aging, and Inhibitory Effect of Vitamin E

Increased F2-Isoprostane Levels in the Rat Brain and Plasma Caused by Oxidative Stress and Aging, and Inhibitory Effect of Vitamin E

Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Ginsenoside Rb1 protects PC12 cells against β-amyloid-induced cell injury

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