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Journal ArticleDOI

Senescence-accelerated-mouse (SAM) : a novel murine model of accelerated senescence

TLDR
The animal model for accelerated senescence named the Senescence-Accelerated Mouse (SAM) was developed in the laboratory (Department ofSenescence Biology, formerly Department of Pathology, Chest Disease Research Institute, Kyoto University) beginning in 1970.
Abstract
n animal model for accelerated senescence named the Senescence-Accelerated Mouse (SAM) was developed in our laboratory (Department of Senescence Biology, formerly Department of Pathology, Chest Disease Research Institute, Kyoto University) beginning in 1970. In this review, the circumstances related to development of SAM, characteristics of aging, pathologic phenotypes, and genetic background of this model are described.

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Mutation of the mouse klotho gene leads to a syndrome resembling ageing

TL;DR: A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes in the mouse, and may function as part of a signalling pathway that regulates ageing in vivo and morbidity in age-related diseases.

Mutation of the mouse klotho gene leads to a syndrome resembling ageing

TL;DR: A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes in the mouse, including short lifespan, infertility, arteriosclerosis, skin atrophy, osteoporosis and emphysema as mentioned in this paper.
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The antioxidants alpha-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice.

TL;DR: The hypothesis that oxidative stress can lead to cognitive dysfunction and provide evidence for a therapeutic role for antioxidants is supported and the hypothesis that antioxidant treatment can reverse cognitive dysfunction is supported.
Journal ArticleDOI

Protective effects of melatonin in reducing oxidative stress and in preserving the fluidity of biological membranes: a review

TL;DR: The present work reviews the current information related to the beneficial effects of melatonin in maintaining the fluidity of biological membranes against free radical attack, and discusses its implications for ageing and disease.
Journal ArticleDOI

Changes in the structural complexity of the aged brain

TL;DR: Findings suggest that age‐related neuronal dysfunction, which must underlie observed decline in cognitive function, probably involves a host of other subtle changes within the cortex that could include alterations in receptors, loss of dendrites, and spines and myelin dystrophy, as well as the alterations in synaptic transmission.
References
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Journal ArticleDOI

On the Nature of the Function Expressive of the Law of Human Mortality, and on a New Mode of Determining the Value of Life Contingencies

TL;DR: The frequent opportunities I have had of receiving pleasure from your writings and conversation, have induced me to prefer offering to the Royal Society through your medium, this Paper on Life Contingencies, which forms part of a continuation of my original paper on the same subject, published among the valuable papers of the Society, as by passing through your hands it may receive the advantage of your judgment.
Journal Article

Development of a Strain of Spontaneously Hypertensive Rats

Kozo Okamoto, +1 more
- 01 Jan 1963 - 
TL;DR: The incidence of the spontaneous occurrence of hypertension increased, the development of hypertension occurred at younger ages from generation to generation, and all of the F3 to F6, rats developed spontaneous hypertension within 15 weeks of age.
Journal ArticleDOI

Development of a strain of spontaneously hypertensive rats.

TL;DR: Okamoto-Aoki et al. as discussed by the authors found that the spontaneous occurrence of hypertension increased with age and the development of hypertension occurred at younger ages from generation to generation, increasing significantly above those of normotensive controls of the same age.
Journal ArticleDOI

Fluorometric determination of amyloid fibrils in vitro using the fluorescent dye, thioflavin T1.

TL;DR: Fluorescence intensity in the presence of a constant amount of amyloid fibrils reached a plateau with increase in the thioflavine T concentration, and the fluorescence was considerably diminished when structure of the amyloids fibril was disrupted by guanidine-HCl treatment.
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