SENS is a practical, foreseeable approach to curing aging because all the types of metabolic side-effect whose accumulation is (or is even hypothesised to be) eventually pathogenic are amenable to repair (or in some cases obviation, i.e. disruption of the mechanism by which they become pathogenic) by techniques that, according to the experimentalists who have performed the key work on which those techniques build, can (with adequate funding) probably be implemented in mice within a decade or so. There are seven major categories of such damage, listed below, along with the leading technique or techniques that can address them. Follow the links to read more detail about these techniques. I apologise that these more detailed pages do not yet include references to the literature. In most cases you can find the key references in my relevant publications, which are all available here.

Note: The dates given are when the category of damage in question was first proposed, in the gerontology literature, to be responsible for aging or some major age-related cause of death or debilitation. The earlier ones may not in fact be the first such mention, but they are well-known and often cited as pioneering publications in the area in question. The full citations are below the table. The relevance of these dates is that they are all over 20 years ago. The fact that we have not discovered another major category of even potentially pathogenic damage accumulating with age in two decades, despite so tremendous an improvement in our analytical techniques over that period, strongly suggests that no more are to be found -- at least, none that would kill us in a presently normal lifetime.

Damage rising with age	Date [ref below]	Reversible or obviatable by [see links for more info]
Cell loss, cell atrophy	1955	Stem cells, growth factors, exercise
Nuclear [epi]mutations (only cancer matters)	1959/ 1982	WILT (Whole-body Interdiction of Lengthening of Telomeres)
Mutant mitochondria	1972	Allotopic expression of 13 proteins
Death-resistant cells	1965	Cell ablation, reprogramming
Extracellular crosslinks	1981	AGE-breaking molecules/enzymes
Extracellular junk	1907	Phagocytosis; beta-breakers
Intracellular junk	1959	Transgenic microbial hydrolases

The above table is to some extent similar to Table 4.3 in Holliday's 1995 book Understanding Ageing, though with important differences resulting from the focus on types of damage rather than types of maintenance. Some of the studies cited here were in fact incorrect in their interpretation of the data they examined, but the point is that they brought the corresponding type of damage to the fore as a candidate component of aging.