Hypothesis: In patients with active rheumatoid disease, senolytic clearance alone will not materially slow epigenetic aging unless it is paired with a mitochondrial rescue intervention. Testable prediction: a sequence of senolytic pulses followed by a brief NAD+ boosting window will outperform senolytics alone on DNAm GrimAge, but only in participants whose baseline mitochondrial stress is high (e.g., elevated plasma GDF15 or mtDNA fragmentation). Mechanism: removing senescent cells should reduce SASP-driven inflammaging, while the post-clearance NAD+ window should restore mitophagy and prevent rebound mitochondrial dysfunction that otherwise continues to drive clock acceleration. Primary endpoint: change in GrimAge acceleration at 16 weeks. Secondary endpoints: GDF15, IL-6, TNF-alpha, circulating cell-free mtDNA, and fatigue score. Falsified if the mitochondrial-stress subgroup does not show a larger clock response than the low-stress subgroup, or if the combination is no better than senolytic alone.