Longevity can be predicted by number of cortical neurons in an animal or so it seems.
https://onlinelibrary.wiley.com/doi/full/10.1002/cne.24564

Crucially, the finding that no correlation between
maximal longevity and metabolic rate remains after accounting for
variation in numbers of cortical neurons argues strongly against
the common notion that damages accumulate at rates that scale
across species depending on metabolism (West et al., 1997).-Herculano Houzel (2018)

Interesting snippet as well as the following

While this new possibility has yet to be investigated, it
leads to one clear prediction: those species with the largest number
of cells in the relevant organ(s) will live longer before succumbing
to physiological breakdown and disintegration and,
consequently, death.-Herculano Houzel (2018)

And yet another related snippet from the news

"The data suggest that warm-blooded species accumulate damages at the same rate as they age. But what curtails life are damages to the cerebral cortex, not the rest of the body; the more cortical neurons you have, the longer you will still have enough to keep your body functional,” said Herculano-Houzel.-source 

But it seems to me that if this were the case you'd see massive lifespan reductions in indivduals with half a brain, which does occur in humans.   Otherwise this would seem to suggest aging may very well be programmed.

Video on programmed aging

In contrast to other oxidative modifications of amino acids, methionine sulfoxide can be enzymatically reduced back to methionine in proteins by the peptide methionine sulfoxide reductase system, composed of MsrA and MsrB. The expression of MsrA and one member of the MsrB family, hCBS-1, was analyzed during replicative senescence of WI-38 human fibroblasts. Gene expression decreased for both enzymes in senescent cells compared to young cells, and this decline was associated with an alteration in catalytic activity and the accumulation of oxidized proteins during senescence. These results suggest that downregulation of MsrA and hCBS-1 can alter the ability of senescent cells to cope with oxidative stress, hence contributing to the age-related accumulation of oxidative damage.-link

Methionine intake has been linked to lifespan, methionine is said to be easily damageable.  Methionine sulfoxide reductases help deal with this damage, yet it seems that senescence results in downregulation of these protective enzymes.   Some say the regular aging process also results in reduction of production of these enzymes, along with the said increase in membrane peroxidation index, the cells would become more damage prone with increasing age.   It is said every ten years, after approx maturity, there's a doubling of mortality.   Why are changes that increase cellular damage taking place?  It's clear that such changes might exceed the maintenance mechanisms of the cells and be behind this increased probability of death.

Programmed aging

In 2002, Severin and Hyman showed that a natural signal molecule (yeast pheromone) sex-specifically kills S. cerevisiae cells [3]. I suggested that this phenomenon can be regarded as a precedent of programmed death of a unicellular organism [4]. Later it was found in our group that the mechanism of such death strikingly resembles apoptosis of higher organisms [5]. To explain the pheromone effect on yeast in terms of the traditional concept of non-programmed death of organisms, Kirkwood and Melov [1] assumed that yeast cells form in fact a multicellular organism. Such an explanation is hardly sufficient since (i) programmed death phenomena are now also described in bacteria [6-9] and (ii) an additional function of a pheromone as an inducer of the organism's death program was discovered in a mammal, the small marsupial Antechinus stuartii.Male of this rodent uses pheromone to attract females and then to kill himself after run [10]. To define all cases of programmed death of organisms, in 1997 I suggested the term "phenoptosis" [11] (for discussion, see [7,9,12]).-link

Article on programmed aging theories.   In the above snippet, we see that in unicellular organisms and in some multicellular organisms programmed death can occur, strengthening the case for aging being programmed.