Whether diseases themselves can accelerate aging is a hypothesis many researchers are currently considering

Whether diseases themselves can accelerate aging is a hypothesis many researchers are currently considering. It is important to remember that nonfatal maladies of aging, such as increased joint pain, loss of vision and hearing, and muscle weakness, should not be neglected, as they have become particularly important in recent times. == Introduction == The geroscience hypothesis, that aging is the major modifiable risk factor for most chronic diseases, is currently well accepted and it is being tested in multiple models and systems, ranging from basic biology in a variety of organisms to preclinical and clinical studies. Aging has been recognized for years as a major risk factor for most chronic diseases that affect the aged population. However , it has traditionally been overlooked as a nonmodifiable risk factor, and thus neglected in most of our approaches to medicine. This has changed recently because of the recognition, among basic biology of aging researchers, of a limited number of pillars that seem to be the main drivers of the aging process. Identification of these pillars was made possible by a multi-pronged approach based on the now classical tenets of aging biology: caloric restriction, cell senescence, and free radicals. While the initial theories and concepts driving each of these fields have been subjected to modifications and redefinitions, research based on these tenets has allowed researchers to identify the major drivers of the process. This in turn has led to the beginnings of efforts aimed at translating the findings through the use of pharmacological approaches aimed at one or more of the pillars of aging, with the hope that, by addressing these fundamental drivers, a positive impact might be achieved in combating not one but multiple chronic diseases in parallel. On the other hand, it is well established that aging and disease susceptibility are highly variable among individuals within the human population, most likely due to variations in the well-known interactions between genes and environment. Against this background, a major environmental variable known epidemiologically to affect the rate of aging (colloquially understood, as there is no agreed-upon definition or measure for the rate of aging) is exposure to early serious disease. It has been well established, at the epidemiological level, that early exposure to severe diseases and/or their treatments leads to an acceleration of aging, as defined by an increased and premature risk of developing diseases and conditions that are associated with increased age. In order to narrow the discussion, in the Second Geroscience Summit, held on April 1314, 2016 in New York, New York, we focused on three examples: cancer, HIV/AIDS, and diabetes. This was driven NCH 51 simply by the need to limit the scope of the discussions, but it is expected that the issues raised will apply, with modifications, to all or most diseases that, while curable, nevertheless leave sequelae that are likely to affect later increased susceptibility to age-related diseases and conditions. That serious diseases and/or their treatments lead to an acceleration of disease susceptibility later in life is well established at the epidemiological level. The goal of the summit was to dig further and try to assess possible molecular and cellular mechanisms that might be responsible for the epidemiological observations. A specific emphasis was placed on links between diseases and/or treatment and the major pillars of aging, with the assumption that if these early life events affect NCH 51 some of the same pillars that have been associated with aging, then this should be a good place to start addressing NCH 51 the relationship between the two. == Geroscience as a multidisciplinary approach to understanding aging == == Richard J. Hodes == The extramural program of the Rabbit Polyclonal to PKC delta (phospho-Ser645) National Institute on Aging (NIA) at the National Institutes of Health (NIH) is organized around four divisions, and each is poised to make unique and substantive contributions to the field of geroscience. The Division of Aging Biology is the lead for geroscience at the NIA, and its focus is on the basic biochemical, genetic, and physiological mechanisms underlying the process of aging and age-related changes in humans and in animal models of human aging. Geroscience is a natural extension of this work. NCH 51 The Division of Neuroscience focuses on the dementias of old age, as well as understanding the processes associated with the normally aging brain. The basic science research funded by this division intersects with geroscience in the areas of biologic mechanisms of disease (e. g., dementias) and age-related changes in the brain that lead to increased disease risk. The Division of Behavioral and Social Research explores aging at the individual and the societal leveland research in areas like.