By Vincent J. Cristofalo PhD
This quantity provides a transparent, concise evaluation of the present kingdom of information concerning the biology of getting older √± serving as either a useful graduate-level textual content and a key reference for training execs. Over a dozen exotic participants probe the newest advancements in our wisdom of why humans age and the way the method works. those authoritative chapters usually are not simply written for biologists √± yet for gerontologists typically. Marks the 10th anniversary of the once a year overview of Gerontology and Geriatrics.
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Extra info for Annual Review of Gerontology and Geriatrics, Volume 10, 1990: Biology of Aging
229-244). New York: Plenum Press. Brown, W. , Kieras, F. 1985. Progeria: A model disease for the study of accelerated aging. In A. Woodhead, A. D. Blackett, & A. ), Molecular biology of aging (pp. 375-396). New York: Plenum Press. Burger, P. , & Vogel, S. 1973. The development of the pathologic changes of Alzheimer's disease and senile dementia in patients with Down's syndrome. American Journal of Pathology, 73, 457-468. GENETIC DISEASES OF PREMATURE AGING 39 Cleaver, J. E. 1982. Normal reconstruction of DNA supercoiling and chromatin structure in Cockayne syndrome cells during repair of damage from ultraviolet light.
Journal of Cellular Physiology, 92, 365-374. Glueck, C. , Fallat, R. , & Steiner, P. M. 1976. Longevity syndromes: Familial hypobeta and familial hyperalpha lipoproteinemia. Journal of Laboratory and Clinical Medicine, 88, 941-957. , Lerman, J. , McBride, O. , & Gajdusek, D. C. 1987. Characterization and chromosomal localization of a cDNA encoding brain amyloid of Alzheimer's disease. Science, 235, 877-880. Goldstein, S. 1969. Lifespan of cultured cells in progeria. Lancet, 1, 424. , & Moerman, E.
Goldstein and Moerman (1975) reported finding an increased fraction of abnormally thermolabile enzymes, including glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and hypoxanthine phosphoribosyltransferase, in progeria fibroblasts. Based in part on the Orgel error-catastrophe hypothesis of aging (1963), it was suggested that diseases resembling premature aging may be the result of widespread errors in protein synthesis (Goldstein & Moerman, 1976). Abnormally high thermolabile enzyme levels in circulating erythrocytes from one progeria patient with intermediate levels in the parents was also reported (Goldstein & Moerman, 1978).