Ageing

The Engineer's Viewpoint: Treat Change as Damage and Fix It

An aging body has changed in many ways, and not just in those obvious to visual inspection. The typical old body is identifiably different from the typical middle-aged body at the level of cells, genes and biochemistry: biochemical processes, gene expression, levels of molecular damage, cellular behaviors, cellular populations, and so on. Some of these differences are clearly causally linked - a wide range of age-related changes can often be shown to be caused by a lesser number of underlying changes. For example, damage to mitochondria leads to oxidization of low-density lipoproteins (LDL), which in turn leads to detrimental changes involved in atherosclerosis, which is the principal cause of coronary heart disease and other forms of cardiovascular disease.

Can ageing be stopped?

Old age hardly exists in wild animals. Accident, illness or predation usually kill long before the potential lifespan has been reached. Humans, though, especially in the developed world, are pushing in ever larger numbers towards the maximum lifespan, thought by most gerontologists to be around 120. In Britain in 1901, life expectancy at birth was 49 for women and 45 for men. By 2002, this had risen to 81 and 76 respectively.

Aubrey de Grey - Prospects for extending healthy life - a lot

It may seem premature to be discussing approaches to the effective elimination of human ... all aging as a cause of death at a time when essentially no progress has yet been made in even postponing it. However, two aspects of human aging combine to undermine this assessment. The first is that aging is happening to us throughout our lives but only results in appreciable functional decline after four or more decades of life: this shows that we can postpone the functional decline caused by aging arbitrarily well without knowing how to prevent aging completely, but instead by increasingly thorough molecular and cellular repair. The second is that the typical rate of refinement of dramatic technological breakthroughs is rather reliable (so long as public enthusiasm for them is abundant) and is fast enough to change such technologies (be they in medicine, transport, or computing) almost beyond recognition within a natural human lifespan. In this talk I will explain, first, why (presuming adequate funding for the initial preclinical work) therapies that can add 30 healthy years to the remaining lifespan of healthy 55-year-olds may arrive within the next few decades, and, second, why those who benefit from those therapies will very probably continue to benefit from progressively improved therapies indefinitely and thus avoid debilitation or death from age-related causes at any age.

Video, 1 hour 1 min

What if Humans were Designed to Last?

When Michelangelo painted The Creation of Adam on the ceiling of the Sistine Chapel, he portrayed the Renaissance view of humanity as having been molded by the hand of its creator, a "perfect" physical specimen. Charles Darwin, when drafting his theory of evolution, presented imperfections in humans' anatomic structures and functions as the strongest evidence for his theory. It now appears they were both right. Subtle changes and imperfections at every level of biological organization give rise to the diseases and disorders associated with aging and impose limits on the duration of life, but ultimately, these changes and imperfections drive the evolutionary process itself. We asked experts in gerontology, neuroscience, genetics, cell biology, development, and health and fitness science to devise a human that would stand the test of time. Here's what they've come up with.

Telomere shortening and cardiovascular disease

One of my favorite new stories in the biology of aging is the body of work demonstrating an unexpected (to my mind, anyway) relationship between telomere length and various “organism-scale�? phenomena, e.g., psychological stress and cardiovascular disease (CVD). Two recent reviews extend the discussion. Kajstura et al. focus directly on cellular senescence, which can be induced both by telomeric shortening and genotoxic damage, in cardiac progenitor cells. Does senescence play a role in cardiovascular aging and the age-related onset of CVD?

Atomic Tune-Up: How the Body Rejuvenates Itself

For most people, a makeover means losing weight and getting new clothes, hair and makeup. But what they may not know is that the body does its own extreme makeover regularly. In fact, 98 percent of the atoms in the body are replaced yearly. Researchers in the 1950s made the discovery by feeding their subjects radioactive atoms. Using radiation detectors, the researchers watched the atoms move all over the body. They found that the new atoms replaced old ones and ended up in all tissues of the human body. But these atomic makeovers prompt a more philosophical question: Are people really themselves if their atoms are always new, or are they new people each year?

Audio, 5 min

10 Easy Paths to Self Destruction

A "Top 10" List

Stress May Promote Aging of Cells

Chronic psychological stress is associated with accelerated shortening of the caps, called telomeres, on the ends of chromosomes in white blood cells -- and thus hasten their demise. Telomeres promote chromosome stability, Dr. Elissa S. Epel at the University of California, San Francisco, and her colleagues explain. Telomeres shorten with each replication of the cell, and cells cease dividing when telomeres shorten sufficiently.

Telomere Length May Predict Heart Disease Risk

Size does matter: Men with short telomeres -- strips of DNA at the end of chromosomes -- may have a higher risk of developing coronary heart disease. And those same men may benefit the most from treatment with cholesterol-lowering drugs known as statins, a new British study found.