Altered nicotinamide adenine dinucleotide metabolism drives cartilage degeneration and osteoarthritis

Wu X, et al. · Clinical and Translational Medicine

NAD+ was depleted in OA cartilage; restoring it with NAD+ precursors (including NMN) or NMNAT1 overexpression suppressed cartilage disruption and matrix-degrading changes in rodent OA models.

Population

Human OA cartilage tissue plus ageing and post-traumatic OA mouse/rat models and cultured chondrocytes

Intervention

NAD+ precursors: nicotinamide riboside 200 mg/kg by mouth daily for 8 weeks in surgical rat OA, and NMN 0.5 or 2 g/L in drinking water for 4 weeks in 13-month-old mice; NMNAT1 overexpression; PARP14 knockdown

Comparator

Untreated OA animals/cells

Limitations

Rodent and in-vitro efficacy only, six animals per group; doses and routes not comparable to human oral supplementation; very recent, not independently replicated. The senior author is a co-founder, shareholder and consultant of two companies developing NAD boosters, and the key mouse experiments were in part funded by one of them.