Alzheimer's disease (AD) is linked to aging and errors in how our genes are processed, a mechanism known as dysfunctional alternative RNA splicing (ASEs). The metabolite NAD+ is known to slow AD progression in preclinical studies.
This 2025 study in Science Advances provides a new mechanism . Researchers found that NAD+ augmentation corrects these harmful splicing errors. It appears to do this by regulating a key protein called EVA1C, which the study found is reduced in the hippocampus of human AD patients compared to cognitively normal ones.
Using mouse models with AD-like tau pathology , supplementing with NAD+ precursors (like NR or NMN) improved memory . Critically, when the researchers blocked the EVA1C protein (via adeno-associated virus-based knockdown) in the mice's hippocampus, the memory improvements from NAD+ were lost .
This suggests the NAD+-EVA1C splicing axis is a critical pathway for how NAD+ protects the brain, offering a potential new target for future AD therapies.
3. Disclaimers
• This information is for educational purposes only and should not be interpreted as medical advice.
• The study discussed was conducted on human cells , C. elegans (worms) , and mouse models . Further research is needed to confirm these specific mechanisms in humans.
• Always consult with a qualified healthcare professional before making any changes to your diet, supplement regimen, or treatment plan, especially if you have a medical condition or are taking medications.
Ai R, Mao L, Jin X, et al. NAD+ reverses Alzheimer's neurological deficits via regulating differential alternative RNA splicing of EVA1C. Sci Adv. 2025;11(eady9811).
#AlzheimersResearch #NAD #EVA1C #RNASplicing #Neuroscience
NAD+, Alzheimer's disease, EVA1C, alternative RNA splicing, ASEs, hTau.P301S, C. elegans, neuroprotection, neurological deficits, memory improvement, nicotinamide adenine dinucleotide, nicotinamide riboside, nicotinamide mononucleotide, tauopathy, hippocampus, spliceosome, neuronal resilience, transcriptomics, Science Advances, Ai et al 2025, HSP70, BAG1, gene regulation, NAD+-EVA1C splicing axis, neurodegeneration