That’s true of NAD itself. These supplements are NAD precursors...
“While direct NAD+ supplementation is not effective due to poor absorption, precursors such as NR and NMN are more bioavailable and have been shown to increase NAD+ levels in the blood.”
Ok, I will put it this way, as the science especially for humans is incomplete. Some get past the blood brain barrier/CNS and some don’t. “Are these NAD+ precursors effective?”
If “effective” means raising NAD+ levels, then several precursors (NR, NMN, nicotinamide/niacin) are effective, at least in blood and, for NR and nicotinamide, with evidence of CNS penetration and increased brain NAD+ in humans or animals.
If “effective” means proven improvement in human cognition, prevention of neurodegeneration, or clear functional brain outcomes, the data are preliminary, often small, and not yet definitive.
Nicotinamide riboside (NR)
Multiple human trials show NR (typically 1,000–3,000 mg/day) raises blood NAD+ 2–3 fold and is well tolerated, and in Parkinson’s disease (NADPARK/NR‑SAFE) it also raised cerebral NAD+ and modestly improved clinical motor scores.
In older adults with mild cognitive impairment, NR increased NAD+ but did not significantly improve overall cognition over 10–12 weeks, though some exploratory measures (e.g., executive function, fatigue, sleep quality) showed within‑group improvements.
Nicotinamide mononucleotide (NMN)
In animal models, systemic NMN after cardiac arrest increased brain NAD+ and ATP, upregulated SIRT3, and improved neurological scores and survival, indicating neuroprotection when given acutely.
Human data on brain‑specific outcomes are sparse; ongoing and early trials mainly assess systemic metabolic or aging markers, so “effectiveness” for human brain health remains speculative.
Niacin / nicotinamide (NAM)
Preclinical work shows NAM can cross into the CNS and protect neurons in models of Huntington’s disease, glaucoma, and oxidative stress, often by boosting NAD+ and reducing apoptotic signaling.
A large, definitive human neuroprotection trial is still lacking; glaucoma trials with high‑dose NAM are underway, but results are not yet conclusive for broad brain indications.
Practical bottom line
There is solid evidence that NR, NAM, and NMN can raise NAD+ and show neuroprotective effects in animals, and NR/NAM demonstrably affect brain NAD+ or neuro-ophthalmic measures in early human work.
However, no NAD+ precursor currently has robust, long‑term human data proving it slows normal brain aging or clearly prevents/halts common neurodegenerative diseases, so any use right now is best viewed as experimental or adjunctive rather than established therapy.