Abstract
It has been long appreciated that abnormal glucose, lipid, and bone metabolism, as well as atherosclerosis and neuronal degeneration, are common accompaniments of old age—often present as co-morbidities in the same individual. However, it is only recently that shared molecular pathogenetic mechanisms related to aging per se have been implicated in the development of these conditions. This forward stride is largely due to significant advances in our understanding of the biology of aging, genetic discoveries in animal models and humans, the demonstration of a similar function of the same genes in different organs, and better grasp of integrative physiology and pathophysiology.