Today I'll point out a two open access papers on the mapping of genetics, epigenetics, aging, and age-related disease. There is a lot of this sort of work taking place these days: it is ever easier to raise funding for any sort of work on genetics, and this is the beginning of the age of practical gene therapy. Intervening in the aging process to slow or reverse aging, as opposed to trying to patch over the late stage consequences of specific age-related diseases without actually touching the processes of aging itself, remains a comparatively small initiative within the aging research community. Most funded work on aging goes towards cataloging and mapping, a part of the great life science initiative to produce a comprehensive atlas of living biology from top to bottom: how our cells and tissues work, and how every function of every biological system changes over time, understood all the way down to the roles of individual molecular interactions. This is an enormous project, staggering in scope, with the present vast databases of molecular biochemistry just a sketch of the outline of the whole when held up against the bigger picture. Barring revolutionary advances in automation and computation this project will be nowhere near complete even several decades from now.

To the extent that factions within the scientific community prioritize complete understanding of aging above interventions in aging based on what we do already know, they have decided that no significant progress on lengthening life will be made in our lifetimes. If this view dominates, the future will be much the same as the recent past, in that the steady upward slope of small gains in adult life expectancy will continue, with the bulk of these benefits arising from incidental side-effects of the standard medical approach to late-stage aging and age-related disease. The patches will get better, but a patched and damaged system still fails; the patch can only delay the inevitable. The most important debate in medical research today is between those who prioritize full understanding and slow progress towards slowing aging versus those who want to take the current catalog of known differences between old and young tissue and fix them in advance of full understanding. That will cost a lot less and achieve answers on the relevance of this damage to aging and rejuvenation far more rapidly than any other methodology.

Unfortunately, gathering greater support and adoption of work on biological repair and rejuvenation is still an uphill battle, despite successes in the making such as senescent cell clearance, an approach gathering more attention these days. The majority of research into aging looks a lot more like the open access papers linked here, which is to say it is interesting, largely focused on genetics, generates a lot of data, and is of little practical use in the near term. Altering gene expression levels in the hopes of improving the situation for older people is somewhat like adjusting the fuel balance of a rusted and worn engine in the hopes that it will run a little longer. It misses the point, the direct and most useful thing that could be done to improve matters. The grand map of molecular biochemistry is absolutely something that should be constructed, and will be of great use to the next generation of biotechnologies - but to focus on that entirely is to sacrifice countless lives, when the research and development community could also be building the first generation of therapies that will help bring an end to degeneration aging.

Discover the network mechanisms underlying the connections between aging and age-related diseases

Although our knowledge of aging has greatly expanded in the past decades, it remains elusive why and how aging contributes to the development of age-related diseases (ARDs). In particular, a global mechanistic understanding of the connections between aging and ARDs is yet to be established. We rely on a network modelling named "GeroNet" to study the connections between aging and more than a hundred diseases. By evaluating topological connections between aging genes and disease genes in over three thousand subnetworks corresponding to various biological processes, we show that aging has stronger connections with ARD genes compared to non-ARD genes in subnetworks corresponding to "response to decreased oxygen levels", "insulin signalling pathway", "cell cycle", etc. Based on subnetwork connectivity, we can correctly "predict" if a disease is age-related and prioritize the biological processes that are involved in connecting to multiple ARDs. Using Alzheimer's disease (AD) as an example, GeroNet identifies meaningful genes that may play key roles in connecting aging and ARDs. The top modules identified by GeroNet in AD significantly overlap with modules identified from a large scale AD brain gene expression experiment, supporting that GeroNet indeed reveals the underlying biological processes involved in the disease.

Systematic analysis of the gerontome reveals links between aging and age-related diseases (full text is PDF only)