Most striking to me in the article was the discovery of the genetic mutation
leading to human premature ageing Hutchinson–Gilford syndrome. Indeed, this syndrome must provide some clues into normal human aging, as Cox writes:

However, the lessons from HGPS are likely to extend
widely to normal ageing. For example, Scaffidi and
Misteli have proposed that accumulation of progerin
in normal individuals may be associated with physiological
ageing (Scaffidi and Misteli 2006).

Moving on to another disease of premature aging, Werner Syndrome, David Kipling at Cardiff University has done some interesting work showing the p38 MAP kinase inhibitors can reverse the WS senescent phenotype in vitro.

The conference and the paper covered much more than just developments in these progeriod syndromes, and other topics included detection of senescent cells, DNA stability (including telomere maintenance, DNA repair and nuclear integrity), the IGF axis, and p38 MAPK stress signalling and developmental switches Notch and Wnt.

The full paper can be found here.