Chronic traumatic encephalopathy is a tauopathy resulting from repeated moderate-to-severe traumatic injuries onto the brain, leading to Tau protein abnormal posttranslational modifications, mislocalization, and deposits. Although the spinal cord shares a lot of structural and cellular similarities, most studies of CNS traumatic injuries were conducted onto the brain. In the present project, we emitted the hypothesis that repeated mild contusions onto the spinal cord could similarly exacerbate the tauopathy in a transgenic mouse expressing an aggregation-prone human mutated tau protein (hTauP301S). We set up a subclinical model of mild and twice-repeated spinal cord injury (SCI) in mouse that was characterized for functional and histopathological outcomes. The week following each SCI, hTauP301S mice did not show any detectable motor or sensory impairments. Histological analysis showed a transient astro- and microgliosis, without any neuronal death. In the meantime, serum neurofilament-light levels were transiently increased. Fifteen weeks after last SCI, significant increase in tau phosphorylation for early-stage pathological markers (AT8) was detected in injured mice compared to sham as well as higher microgliosis and higher serum levels of neurofilament-light, the latter being an evidence of neuronal damages. During aging, the decline of the clinical score, forelimb strength and tactile perception was accelerated in the mice that underwent the mild and repeated spinal contusions. These results showed that a mild and repeated spinal cord injury is sufficient to accelerate tauopathy development in a tau aggregation-prone animal model worsening general health state of these animals at long-term.