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Download or read book Supercentenarians written by Heiner Maier and published by Springer Science & Business Media. This book was released on 2010-05-17 with total page 331 pages. Available in PDF, EPUB and Kindle. Book excerpt: Does human mortality after age 110 continue to rise, level off, or start to decline? This book describes a concerted, international research effort undertaken with the goal of establishing a database that allows the best possible description of the mortality trajectory beyond the age of 110. The International Database on Longevity (IDL) is the result of this ongoing effort. The IDL contains exhaustive information on validated cases of supercentenarians (people 110 years and older) and allows unbiased estimates of mortality after age 110. The main finding is remarkable: human mortality after age 110 is flat at a probability of death of 50% per year. The sixteen chapters of this book discuss age validation of exceptional longevity, data on supercentenarians in a series of countries, structure and contents of the IDL, and statistical analysis of human mortality after age 110. Several chapters include short accounts of specific supercentenarians that add life to demographic research.

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Download or read book Polyglutamine Disorders written by Clévio Nóbrega and published by Springer. This book was released on 2018-02-09 with total page 467 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book provides a cutting-edge review of polyglutamine disorders. It primarily focuses on two main aspects: (1) the mechanisms underlying the pathologies’ development and progression, and (2) the therapeutic strategies that are currently being explored to stop or delay disease progression. Polyglutamine (polyQ) disorders are a group of inherited neurodegenerative diseases with a fatal outcome that are caused by an abnormal expansion of a coding trinucleotide repeat (CAG), which is then translated in an abnormal protein with an elongated glutamine tract (Q). To date, nine polyQ disorders have been identified and described: dentatorubral-pallidoluysian atrophy (DRPLA); Huntington’s disease (HD); spinal–bulbar muscular atrophy (SBMA); and six spinocerebellar ataxias (SCA 1, 2, 3, 6, 7, and 17). The genetic basis of polyQ disorders is well established and described, and despite important advances that have opened up the possibility of generating genetic models of the disease, the mechanisms that cause neuronal degeneration are still largely unknown and there is currently no treatment available for these disorders. Further, it is believed that the different polyQ may share some mechanisms and pathways contributing to neurodegeneration and disease progression.

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