In western nations, the average age of spinal cord injury (SCI) has increased and is equally spread out between 20-65 years old. SCI typically causes focal demyelination of spared axons near the site of injury. Surprisingly, we did not find locomotor impairment after SCI when remyelination was inhibited in young mice (Duncan et al. 2018, Nat. Comm). However, the functional impact of remyelination after SCI at an advanced age is unknown. Here, we assessed the importance of remyelination for locomotor recovery, cognitive function, and anxiety in young (3-5 month) and aged (15-18 month) mice of both sexes. To inhibit remyelination we crossed a PDGFRαCreERT2 driver line, which targets oligodendrocyte progenitor cells, with an inducible knockout of the key transcription factor myelin regulatory factor gene (Myrf).The knockout results in the inhibition of oligodendrocyte maturation, thus inhibiting new myelin production. These mice were compared to littermate controls. Mice either underwent a moderate/severe thoracic (T9/10) level contusion or a sham injury and were analyzed with a variety of behavioral tests for 3 months. The aged, injured, remyelination incompetent mice showed delayed locomotor recovery, as assessed through the Basso Mouse Scale, horizontal ladder, and Noldus Catwalk. They also displayed cognitive deficits measured through Y-maze, the object relocation task, and novel object replacement task. No differences were found in terms of anxiety. Overall, the current results suggest that remyelination treatments may have a greater impact in older than in younger individuals with SCI, giving greater insight into the need for personalized therapies post SCI.