Alzheimer’s disease can be reversed in animal models? Study

Study claims and mechanism

• Study reports that P7C3-A20, a small molecule that “restores NAD+ balance,” reversed pathology and cognitive deficits in two advanced transgenic mouse models (amyloid- and tau-based).
• Some see this as promising because it targets cellular energy/NAD+ homeostasis rather than just amyloid, which has a poor track record.
• Others argue the framing (“full neurological recovery,” “reversal of advanced AD”) is overstated marketing language based on narrow mouse readouts.

Mouse models and translational skepticism

• Strong consensus that current Alzheimer’s mouse models are very weak proxies for human disease: mice don’t naturally get Alzheimer’s; they are engineered or poisoned to show similar pathology.
• Commenters note dozens–hundreds of prior “cures” in mice that failed in humans; 5xFAD-style models are seen as particularly bad predictors.
• Some argue these models may actively mislead by optimizing drugs to fix the wrong mechanisms (“low NAD+: fire or ashes?”).

NAD+ precursors, cancer risk, and commercialization

• Study press material warns that OTC NAD+ precursors (NMN, NR, etc.) can raise NAD+ to “dangerously high” levels and promote cancer in animals, whereas P7C3-A20 allegedly restores balance without supraphysiologic levels.
• Several push back: human cancer risk from such supplements is described as unclear or likely very small; claims of superior safety are viewed as speculative preclinical spin.
• Discussion touches on monetization: cheap, ubiquitous precursors vs a patent-protected drug. Method-of-use and formulation patents are explained as standard pharma strategies.

Self-experimentation and access

• P7C3-A20 is already sold by research suppliers in tiny, expensive quantities; some mention group buys for experimental drugs and associated risks (contamination, no effect, serious side effects).
• Multiple comments urge against turning oneself into an unsupervised lab rat, especially given unknown toxicity and lack of human data.

Disease definition and heterogeneity

• Several note that “Alzheimer’s” is likely an umbrella label spanning multiple underlying pathologies (amyloid, tau, vascular, Lewy bodies, mixed cases).
• This heterogeneity may explain why uniform mouse models and one-size-fits-all drugs often fail in humans; precision subtyping is seen as essential.

Ethical tradeoffs and lived experience

• Strong, often visceral discussion comparing Alzheimer’s vs cancer: many would accept a substantial increase in cancer risk to avoid dementia; others stress cancer can involve prolonged, agonizing suffering too.
• Personal stories highlight the financial, emotional, and dignity costs of prolonged dementia, motivating calls for assisted suicide/“dignified death,” tempered by worries about coercion and slippery slopes.

Medicine, diagnostics, and prevention claims

• Broader complaints that medical “debugging” is probabilistic and often shallow; patients with complex chronic issues describe out-performing their doctors in figuring things out.
• One commenter asserts Alzheimer’s is essentially “brain diabetes” from sugar/carbs and “easily avoided”; another strongly disputes this as reductive and blame-shifting, emphasizing that diet is not the whole story.