The latest Nature Reviews Molecular Cell Biology contains a collection of interesting papers on the biology of aging. Interestingly, nothing on the role of oxidative damage or mitochondria in aging, but many of the other major areas of present mainstream biogerontology are covered.

Endocrine regulation of ageing

Over the past 15 years it has become clear that mutations in genes that regulate endocrine signalling pathways can prolong lifespan. Lifespan can be increased by altered endocrine signalling in a group of cells or a single tissue, which indicates that crosstalk between tissues functions to coordinate ageing of the organism. These endocrine pathways might serve as targets for the manipulation of the ageing process and prevention of age-related diseases.

The role of nuclear architecture in genomic instability and ageing

Eukaryotes come in many shapes and sizes, yet one thing that they all seem to share is a decline in vitality and health over time - a process known as ageing. If there are conserved causes of ageing, they may be traced back to common biological structures that are inherently difficult to maintain throughout life. One such structure is chromatin, the DNA-protein complex that stabilizes the genome and dictates gene expression. Studies in the budding yeast Saccharomyces cerevisiae have pointed to chromatin reorganization as a main contributor to ageing in that species, which raises the possibility that similar processes underlie ageing in more complex organisms.

How stem cells age and why this makes us grow old

Recent data suggest that we age, in part, because our self-renewing stem cells grow old as a result of heritable intrinsic events, such as DNA damage, as well as extrinsic forces, such as changes in their supporting niches. Mechanisms that suppress the development of cancer, such as senescence and apoptosis, which rely on telomere shortening and the activities of p53 and p16INK4a, may also induce an unwanted consequence: a decline in the replicative function of certain stem-cell types with advancing age. This decreased regenerative capacity appears to contribute to some aspects of mammalian ageing, with new findings pointing to a 'stem-cell hypothesis' for human age-associated conditions such as frailty, atherosclerosis and type 2 diabetes.

We are complex networks of interacting, self-modifying, slowly damaged systems. Scientists are still in the process of describing human biochemistry in enough detail to manipulate it in ways we would like. Understanding and intervening in the aging process is a task and a half, that much is sure. But what else could be the rational response to suffering and death on a massive scale? We can see that something can be done, and so must act.

Technorati tags: aging, medical research

Posted by Reason at August 24, 2007 9:41 PM | TrackBack (0)