They also performed better in tests of motor function, gait coordination, grip strength and endurance. The findings describe experimental effects in mice and do not demonstrate that NMN can treat spinal cord injury in people. Spinal cord injury can produce localized damage that extends to neighboring cells and tissues over hours, days or weeks, adding to the severity of the initial injury.

Intracellular NAD+ levels decline rapidly during this progression. NAD+ is a coenzyme involved in energy metabolism and other physiological processes, including tissue repair, so depletion of the molecule can adversely affect cells and amplify tissue damage. NMN is a direct precursor of NAD+.

The researchers tested whether increasing NAD+ after spinal cord injury could preserve tissue, restrain the post-injury inflammatory response and support motor recovery. The treatment regimen was 500 mg of NMN per kilogram of body weight, administered by intraperitoneal injection immediately after a moderate contusion-type spinal cord injury and then daily for seven days. Investigators examined spinal cord sections with paraffin hematoxylin-eosin staining to measure vacuole area and with immunofluorescence to assess neuron counts and fluorescence intensity.

The treated animals showed reduced vacuole area and increased neuron counts, indicating less visible tissue disruption under the experimental conditions. The study combined these structural measurements with behavioral assessments rather than examining biochemical changes alone. Motor outcomes were evaluated with the Basso Motor Scale, gait coordination analysis, grip strength assessment and a baton-transfer endurance test.

Mice treated with NMN performed better across these measures after the injury. The convergence between the tissue and behavioral results indicates that the histological protection observed in treated mice was accompanied by improved locomotor performance. Molecular measurements provided a possible explanation for the observed neuroprotection.

Transcriptome sequencing, quantitative reverse-transcription polymerase chain reaction, protein microarray analysis and enzyme-linked immunosorbent assays collectively suggested that NMN attenuated inflammatory responses after injury. Western blot analysis indicated that this effect may have been mediated through the NF-κB pathway. The proposed mechanism is that increasing NAD+ with NMN helps protect injured spinal cord tissue, limits neuroinflammation and thereby supports locomotor recovery.

The researchers described the pathway relationship as a possible mechanism in the mouse model, rather than a demonstrated clinical effect. Overall, the study provides preclinical evidence for NMN as an intervention that may reduce tissue injury and improve motor outcomes following spinal cord injury, while the scope of the reported experiment remains limited to mice tested with a specific dose, route and seven-day schedule.

Subject of Research: Preclinical testing of nicotinamide mononucleotide for spinal cord injury in mice

Article Title: Nicotinamide mononucleotide elevates NAD+ to protect spinal cord tissue from injury and reduces inflammatory response to promote motor recovery

Article References: Zhang, C., Li, Y., Yu, Y., Bai, F., Jing, Y., Talifu, Z., Wang, X., Zhang, X., Li, J., & Cui, G. (2026). Nicotinamide mononucleotide elevates NAD+ to protect spinal cord tissue from injury and reduces inflammatory response to promote motor recovery. BMC Neuroscience. https://doi.org/10.1186/s12868-026-01063-w

Image Credits: AI Generated

DOI: 10.1186/s12868-026-01063-w

Keywords: nicotinamide mononucleotide, NAD+, spinal cord injury, motor recovery, neuroprotection, neuroinflammation, NF-κB pathway, mouse model, contusion injury, tissue damage, Nicotinamide, mononucleotide