🧫 Experiment Protocol
In-VitroAlzheimer diseasePrimary cortical neurons from aged (18-month) mice or SAMP8completed
Evaluate whether NAD+ precursor supplementation (NMN) activates SIRT1/PGC1α signaling, restores mitochondrial function, and reduces senescence markers in aged neurons and senescence-accelerated mouse model (SAMP8).
PRIMARY OUTCOME
NAD+/NADH ratio, SA-β-gal positivity, mitochondrial OCR
EXPECTED OUTCOMES
NMN treatment increases NAD+/NADH ratio >2-fold, elevates SIRT1 activity, reduces SA-β-gal positivity by >40%, and restores mitochondrial oxygen consumption rate (OCR).
SUCCESS CRITERIA
NAD+/NADH ratio (colorimetric assay), SA-β-gal assay, mitochondrial OCR (Seahawk); threshold: p < 0.05 vs. aged vehicle control.
Source: auto-generated