The proliferation of mitochondrial DNA (mtDNA) with deletion mutations has been linked to aging and age related neurodegenerative conditions. In this study we model the effect of mtDNA half-life on mtDNA competition and selection. It has been proposed that mutation deletions ([Formula: see text]) have a replicative advantage over wild-type ([Formula: see text]) and that this is detrimental to the host cell, especially in post-mitotic cells. An individual cell can be viewed as forming a closed ecosystem containing a large population of independently replicating mtDNA. Within this enclosed environment a selfishly replicating [Formula: see text] would compete with the [Formula: see text] for space and resources to the detriment of the host cell. In this paper, we use a computer simulation to model cell survival in an environment where [Formula: see text] compete with [Formula: see text] such that the cell expires upon [Formula: see text] extinction. We focus on the survival time for long lived post-mitotic cells, such as neurons. We confirm previous observations that [Formula: see text] do have a replicative advantage over [Formula: see text]. As expected, cell survival times diminished with increased mutation probabilities, however, the relationship between survival time and mutation rate was non-linear, that is, a ten-fold increase in mutation probability only halved the survival time. The results of our model also showed that a modest increase in half-life had a profound affect on extending cell survival time, thereby, mitigating the replicative advantage of [Formula: see text]. Given the relevance of mitochondrial dysfunction to various neurodegenerative conditions, we propose that therapies to increase mtDNA half-life could significantly delay their onset.