The list was as follows:

Cell loss in brain (Andersen’s session). It has been well publicised that neural progenitor cells have been found in various areas of the brain in recent years. Furthermore, symptoms of Parkinson's disease have been successfully reversed by the implantation of dopaminergic neurons. Sample literature reference: Armstrong et al, Cell Transplantation 9:139-152.

Cell loss in muscle (McCarter’s session). Sarcopenia (loss of muscle mass) is now broadly accepted to comprise both loss of fibre volume and loss of fibre number. However, the debate on how such changes can be reversed is presently very active, as a result of remarkable gains in both fibre volume and fibre number reported to result from suitably regimented exercise. Sample literature reference: Fiatarone et al, JAMA 263:3029-3034.

Cell loss in glands (Bartke’s session). The 30% extension of maximum lifespan by loss of genes involved in growth hormone production is well known to the participants; it is a sterling example of a spectacular breakthrough that was given virtually no airtime in the science media. A recent advance of comparable significance was the nearly complete reversal of thymic involution by IGF-7. Sample literature reference: Aspinall et al, Biochem Soc Trans 28:250-254.

Reversal of the effects of mitochondrial mutations (de Grey’s session). Several ways to achieve this have been advocated in the literature uring the past decade; one very promising approach is introduction into the nuclear genome of suitably modified versions of the 13 protein-coding genes of the mitochondrial DNA. Zullo has recently achieved this (for one gene) in both hamster and human cell culture -- see http://tango01.cit.nih.gov/sig/webversion.pdf for a preliminary account. Sample literature reference: de Grey, Trends Biotechnol 18:394-399.

Reversal of the effect of nuclear mutations and dysdifferentiation (Ames’s session). Several innovative approaches to cancer therapy have been unveiled in recent years; the one gaining most attention is angiostasis, particularly the work of Folkman's group (see e.g. Science 284:808), but others also show promise, including generating antibodies to a patient's own tumour (e.g. Semin Oncol 25:646-653) – which shows particular promise for post-metastatic cancer – and identification of tumour-specific shed proteins (e.g. Yantiri et al, Arch Biochem Biophys 385:336) or mtDNA (Fliss et al, Science 287: 2017) in bodily fluids, which promise earlier diagnosis than yet possible. Changes in the regulation of DNA were proposed long ago by Cutler as a major aspect of aging, due to the maintenance of methylation by copying the methylation state of the other strand, but it is now known to be much subtler – the work of Issa (e.g. Curr Top Microbiol Immunol 249:101-118) shows that sometimes methylation rises with age, and that there is potential for controlling this systemically.

Reversal of decline in cellular proliferative potential (Campisi’s session). This topic is often thought to revolve around telomerase manipulation, which is of course being energetically pursued; less conspicuous aspects of it which have seen recent progress are the response to particular growth factors (see Aspinall et al, above) and (in osteoblasts) to carefully-controlled mechanical stress on bones. Sample literature reference: Swezey et al, J Rheumatol 27:1260-1264.

Reversal of accumulation of cross-linked, unrecycled macromolecules in the extracellular medium and within lysosomes (Cerami’s session). One intervention deserves the most mention here: Alteon's compound, ALT-711, which breaks cross-links in the extracellular space that are due to glycoxidation reactions (Vasan et al, Nature 382:275). Other approaches include transgenic introduction of hydrolytic enzymes of bacteria, which have now been shown to break down lipofuscin (de Grey and Archer, unpublished).

Revival of regenerative capacity present in other vertebrates, which may underlie their negligible senescence (Austad’s session). The regenerative capacity of certain amphibians has been known for centuries; this, however, has mostly been studied in terms of regenerating complex structures such as limbs. Of more fundamental interest to mammalian aging is the way in which negligibly senescing species such as rockfish avoid the various age-related degenerative changes surveyed above. If, for example, they maintain cellular turnover in tissues where we lack it (such as the heart), that tells us that bringing about such turnover is not nearly as challenging as we might otherwise think, given the extremely slight differences at the gene level between different vertebrates. Projects coordinated by John Guerin and presented at the recent AGE meeting have already taken this line of research forward substantially.