NAD+ supplementation improved memory and reduced Alzheimer’s pathology in mice by correcting abnormal RNA splicing patterns through a protein called EVA1C, which was found to be reduced in the hippocampus of Alzheimer’s patients compared to cognitively normal individuals.
This research reveals a previously unknown mechanism for how NAD+ may protect brain function—not just through energy metabolism, but by fixing the molecular ‘typos’ in how genes are read and processed. For those using NAD+ precursors like NMN or NR for cognitive support, this suggests these compounds may work at a more fundamental level of cellular communication than previously understood, potentially addressing root causes rather than just symptoms of cognitive decline.
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Multiple NAD+ clinical trials for Alzheimer’s are currently underway, but scientists have struggled to pinpoint exactly how this metabolite slows disease progression. This study identifies alternative RNA splicing—a process that goes awry with aging—as a key target. The finding that NAD+ effects depend partially on EVA1C opens the door for combination therapies and helps explain why NAD+ augmentation shows such broad neuroprotective effects across different models of cognitive decline.
NAD+ reverses Alzheimer’s neurological deficits via regulating differential alternative RNA splicing of EVA1C
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