Levels of the molecule NAD+ (nicotinamide adenine dinucleotide), essential for cellular energy metabolism, drop sharply in Alzheimer's disease — much more than in normal aging.

Yes, this new research is real and was published very recently (December 22, 2025) in the journal Cell Reports Medicine. It was conducted by scientists from Case Western Reserve University, University Hospitals Cleveland Medical Center, and other institutions, led by Professor Andrew A. Pieper.Key Findings from the Study:

• Mechanism: Levels of the molecule NAD+ (nicotinamide adenine dinucleotide), essential for cellular energy metabolism, drop sharply in Alzheimer's disease — much more than in normal aging. This leads to oxidative stress, inflammation, blood-brain barrier damage, tau protein accumulation, amyloid plaques, neuron loss, and cognitive decline.
• Drug Used: The compound P7C3-A20 does not overly boost NAD+ (unlike some supplements like NMN or NR, which can raise it to unsafe levels and potentially promote cancer). Instead, it helps brain cells maintain natural NAD+ balance under stress.
• Results in Animal Models:
  • Tested on two mouse models: 5xFAD (amyloid-focused) and PS19 (tau-focused).
  • When given early, it prevented disease progression.
  • Remarkably, when started in mice with advanced, severe disease, it fully reversed pathology: reduced inflammation, repaired blood-brain barrier, lowered oxidative stress and DNA damage, restored synapse loss and hippocampal neurogenesis.
  • Memory and cognitive function fully recovered (e.g., normal performance in Morris water maze tests).
  • Blood levels of the key Alzheimer's biomarker p-tau217 normalized (this is a marker used in human diagnostics).
• Human Brain Analysis: In postmortem human brains, severe Alzheimer's showed disrupted NAD+ balance. Interestingly, some people with Alzheimer's pathology but no dementia symptoms had preserved NAD+ balance, suggesting it's protective.

This is a breakthrough because it demonstrates complete reversal of advanced Alzheimer's in models, not just prevention or slowing — something rarely achieved before.Important Caveats:

• This is preclinical — only in mice and human tissue analysis. Mouse models capture aspects of Alzheimer's but not the full human disease.
• P7C3-A20 is experimental and not approved for human use. Human clinical trials are needed.
• The authors strongly warn against self-medicating with NAD+ boosters (e.g., NMN, NR supplements), as they can elevate NAD+ too high and increase cancer risk in animal studies.

Your original post accurately reflects the study's press release and findings. It's an exciting development offering hope, but we're still years away from potential human treatments. We'll need to watch for upcoming clinical trials!