Nicotinamide Riboside (NR) for ALS
Also known as: NR, Niagen, TruNiagen
NAD+ depletion accelerates motor neuron degeneration in ALS, and NR is a potent NAD+ precursor.
Mechanism of Action
NR is phosphorylated by NR kinases to NMN, then converted to NAD+. Elevated NAD+ activates SIRT1/3 for mitochondrial protection, enhances PARP1-mediated DNA repair in motor neurons, and supports axonal NAD+ pools critical for motor neuron viability.
General mechanism: NAD+ precursor via NR kinase pathway. SIRT1/3 activator, mitochondrial biogenesis enhancer, PARP1 substrate, DNA repair support.
Current Evidence
Preclinical ALS models show benefit from NAD+ augmentation. Human trials in other neurodegenerative conditions inform dosing. ALS-specific trials planned.
Clinical Status: Preclinical for ALS. Phase II for other neurological conditions. Available as supplement.
Safety Profile
Very safe at 300-1000mg/day. Mild GI effects. Well-tolerated in clinical trials. No significant drug interactions.
Key Research Questions
- Does NR-mediated NAD+ restoration slow motor neuron degeneration?
- Can NR support axonal NAD+ in long motor neuron axons affected in ALS?