Abstract: Spinal cord injury (SCI) is a debilitating condition resulting in varying degrees of functional impairment and exhibits only limited repair. Currently there is no cure for SCI, and no proven treatment to promote restoration of function. One area that has received extensive attention, with the goal of promoting functional recovery, is promoting axonal regeneration and growth in the injured cord. However, one factor that is likely to impede the translation of promising restorative therapies from the bench to the clinic is the lack of consideration of the aging factor in SCI research and its impact on axon regeneration in particular. In the United States, the average age of occurrence of SCI is 43 years old (National Spinal Cord Injury Statistical Center), with a peak in incidence in young (20–30 years) and in aging (≥ 65 years) adults (GBD 2016 Traumatic Brain Injury and Spinal Cord Injury Collaborators, 2019). Patients are also living longer with the injury, with approximately 80% of all people with a SCI being over 40 (One Degree of Separation, Christopher & Dana Reeve Foundation). This demographic change has largely not been addressed in pre-clinical research. Indeed, the bulk of pre-clinical research is performed in young adult rodents (2–4 months), despite 6 month old mice more appropriately representing the 20–25 year old population in humans, and less than 0.35% of experimental rodents being 12 months or older, mimicking 40 years of age in humans (Fouad et al., 2020). In fact, an age-dependent decline in axon growth has been reported in a variety of model organisms, mediated by both neuron-intrinsic (Geoffroy et al., 2017) and extrinsic mechanisms (Sutherland and Geoffroy, 2020). While there has been significant progress made in understanding and manipulating axon growth after injury, even genetic manipulations promoting growth seem age-sensitive (Geoffroy et al., 2017), suggesting that other factors are needed to enhance axon growth in aging neurons. One of these factors is mitochondria. The mitochondrial theory of aging is one of the main mechanisms proposed to explain the biological process of aging. With age, mitochondrial function is reduced, which has been associated with a wide range of age-related diseases, including neurodegeneration (Haas, 2019). Importantly, mitochondria are essential for axonal growth and cell maintenance. Both normal aging and traumatic injury to the central nervous system (CNS) are highly associated with mitochondrial dysfunction and oxidative stress, this poses a great challenge for an aging SCI population as the two elements can compound one another to worsen injury outcomes. Observations from our laboratory has found detrimental changes in mitochondria in the aging CNS across a range of functional areas that will have a significant effect on neuronal health and ability to promote axonal growth in the event of injury. These observations suggest an important role for mitochondria in the age-dependent decline in axon growth potential that has been previously observed, and also may suggest targeting mitochondria as a promising therapeutic avenue for SCI regardless of age.