Normal aging in humans and rats is associated with a decline in food intake and body weight (BW)(1). This condition is defined asanorexia of aging'and is considered a physiological phenomenon of normal aging; nevertheless this anorexia is often responsible for undernutrition and consequent physical deterioration (2). In fact, long-term tissue catabolic processes significantly reduce not only body fat, but also lean body mass, leading to osteoporosis, sarcopenia, impaired immunity and parenchymatous organ failure. These pathological events worsen quality of life and shorten life span (1).

A variety of studies indicate that age-related anorexia is associated with alterations in the homeostatic mechanisms controlling hunger and satiety in the central nervous system. An important role in the pathogenesis of anorexia of aging has been attributed to age-related changes in the leptin±NPY (neuropeptide Y) feeding pathway. Particularly, reduction in function and content of NPY in several cerebral areas has been demonstrated during advanced ages in rats (for review see 1). These demonstrations required the use of invasive methods, and thus could not be confirmed in the human species. In recent years, it has become possible to measure plasma circulating levels of NPY and leptin in humans. Therefore, we decided to measure these neurochemicals in the blood of senescent human subjects to verify whether significant