Catálogo de publicaciones - revistas

<jats:p> <jats:bold>Why We Age.</jats:bold> What Science Is Discovering About the Body's Journey Through Life. STEVEN N. AUSTAD. Wiley, New York, 1997. xii, 244 pp., illus. $24.95, C$34.95, or £19.99. ISBN 0-471-14803-2. </jats:p> <jats:p> <jats:bold>Between Zeus and the Salmon.</jats:bold> The Biodemography of Longevity. KENNETH W. WACHTER and CALEB E. FINCH, Eds. National Academy Press, Washington, DC, 1997. viii, 312 pp., illus. $44 or £35.95. ISBN 0-309-05787-6. To be published 3 November. </jats:p>

<jats:p>The role of genetics in determining life-span is complex and paradoxical. Although the heritability of life-span is relatively minor, some genetic variants significantly modify senescence of mammals and invertebrates, with both positive and negative impacts on age-related disorders and life-spans. In certain examples, the gene variants alter metabolic pathways, which could thereby mediate interactions with nutritional and other environmental factors that influence life-span. Given the relatively minor effect and variable penetrance of genetic risk factors that appear to affect survival and health at advanced ages, life-style and other environmental influences may profoundly modify outcomes of aging.</jats:p>

<jats:p>Neurodegenerative disorders are characterized by extensive neuron death that leads to functional decline, but the neurobiological correlates of functional decline in normal aging are less well defined. For decades, it has been a commonly held notion that widespread neuron death in the neocortex and hippocampus is an inevitable concomitant of brain aging, but recent quantitative studies suggest that neuron death is restricted in normal aging and unlikely to account for age-related impairment of neocortical and hippocampal functions. In this article, the qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored. When these data are viewed comprehensively, it appears that the primary neurobiological substrates for functional impairment in aging differ in important ways from those in neurodegenerative disorders such as Alzheimer's disease.</jats:p>