This popular science article examines a few of the current efforts to build the foundation for therapies to treat aging and its consequences, with a particular focus on parabiosis research in which the circulatory systems of old and young individuals are linked. This approach is being used to investigate differences in levels of gene expression that occur with age, most likely in reaction to rising levels of cell and tissue damage, and especially those changes connected to decline in stem cell function. A promising sign for the near future of advocacy for longevity science is that journalists, such as the author of this piece, are starting to understand the importance of treating the root causes of aging and age-related disease, rather than focusing on each disease of aging in its late stages and trying to patch over the consequences.
First, let's go over what will happen to us as we grow old. Sometime after age 50, depending on personal genetics and life history, our gums withdraw, we lose our hair, our saliva glands falter, and our teeth grow brittle and break off or fall out. Our skin gets thinner, less flexible; it sags, wrinkles, and is discolored by "liver spots." Our bones lose density and strength and shrink in size as our joints swell. Our shoulders slump, our spines buckle and hump. Our muscles atrophy and waste away so we lose mobility as we grow progressively weaker. Our balance and hearing deteriorate. Our eyes dry and lose their ability to focus, so we're more likely to fall, and our bones break more easily. We're slower to heal and more vulnerable to infection as we do, if we do. Hormone levels change. Our memory fails, and most of us, almost all of us, will develop dementia if we live long enough.
Living until 120, the life-span traditionally attributed to Moses, seems more like a curse than a blessing. But it doesn't have to be that way. I've spent the last year talking with scientists around the world about why we've been so successful treating the diseases of youth and middle age and yet haven't made similar progress against end-of-life afflictions. What I found is that scientists at Stanford, Harvard, USC, Wake Forest, UC Berkeley, San Francisco, USC, and Cambridge University, at Scripps Institute, the SENS Research Foundation, and Buck Institute for Research on Aging are unanimous in agreement: Science has gained the ability to intervene successfully in the aging process and to delay and to selectively reverse its effects. The speed at which these new technologies and techniques - which now exist - move from the lab to the clinic is directly dependent on public awareness and support.
Scientists have traditionally studied diseases separately because they have separate pathologies. Heart disease mostly comes from accumulated fat deposits clogging arteries, cancers from DNA damage, Alzheimer's and other dementias from damaged brain cells, etc. - and each disease has multiple contributing factors. But they share a common feature: Aging drives them all. If we delay aging and rejuvenate organs, tissues, and cells, we can prevent or remediate them all. Although aging is the major risk factor for developing most adult-onset diseases, systematic investigations into the fundamental physiology, biology, and genetics of aging are only just beginning. Yet there's good reason to be confident that moving away from the "infectious disease" model and shifting research dollars from individual diseases of aging to the basic biology of aging will be productive.