By Nozomu Mori, Inhee Mook-Jung
This ebook brings jointly the main updated details on contemporary study result of top laboratories on getting older technological know-how in East Asia, really in Japan, Korea, and Hong Kong. beginning with a finished evaluate of varied hypotheses on organic mechanisms of getting older by way of Dr. Sataro Goto, each one bankruptcy covers extensive facets of the latest findings in aging-related themes: centenarian reviews and genome research of progeria, metabolic biochemistry and neurobiology, toughness controls in yeast and nematodes, oxidative tension and calorie restrict, and neurodegeneration mechanisms in Alzheimer’s and Huntington’s illnesses, with additional strength healing ways to those age-related neurodegenerative ailments. additionally integrated, partially, is a precis and the results of a systematic dialogue discussion board referred to as the Asian getting older middle for sturdiness (AACL) that has been held each year alternating among Japan and Korea over the past decade. This ebook can function an invaluable source for locating acceptable collaborators within the parts it covers. the objective readership is made of graduate scholars and researchers at universities, scientific and/or life-science faculties, and biomedical and pharmaceutical institutes.
Why does getting older exist? How can we age? How is every one organism’s lifespan decided? those are basic questions within the box. We will be nonetheless faraway from attaining an entire view of getting older mechanisms, yet this e-book, Aging Mechanisms, deals an exceptional chance to familiarize yourself with the main up-to-date growth within the biomedical study of getting older in Japan and Korea, the 2 best countries for human longevity.
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Additional info for Aging Mechanisms: Longevity, Metabolism, and Brain Aging
The thickness of the intima-media complex (IMT) and the prevalence of plaque in the carotid artery were assessed. We found that the IMT increases linearly with age. 83). However, the prevalence of plaque showed a different trend. Plaque begins to appear after 50 years of age and then increases in prevalence linearly with the highest prevalence observed among nonagenarians. 6 % in octogenarians). The regression of plaque does not usually take place. We hypothesize that the nonagenarians with severe atherosclerosis may die before 100 years of age and that a low prevalence of clinically demonstrable atherosclerosis is critical to attain 100 years of age.
J Biol Chem 277: 44784–44790 1 The Biological Mechanisms of Aging: A Historical and Critical Overview 27 Strehler BL (1977) Time, cells and aging. Academic, New York Strong R, Miller RA, Astle CM, Baur JA, de Cabo R, Fernandez E et al (2013) Evaluation of resveratrol, green tea extract, curcumin, oxaloacetic acid, and medium-chain triglyceride oil on life span of genetically heterogeneous mice. J Gerontol A Biol Sci Med Sci 68:6–16 Subba Rao K, Martin GM, Loeb LA (1985) Fidelity of DNA polymerase-beta in neurons from young and very aged mice.
There are many other examples of protein misfolding and aggregation causing age-related diseases (Stefani 2004). While numerous cases, especially in neurodegenerative diseases, have been reported in which protein alterations produce age-related pathologies, it is not clear whether such changes also contribute to the functional decline of cells and tissues in physiological aging. It is possible that minor alterations of individual proteins cause undetected changes, yet result in significant physiological deterioration during aging.