P7C3-A20 drug reverses the effects of Alzheimer’s disease in mice
By Anni Yurcisin. This article was initially published in the 1/29/26 Edition of our Concussion Update newsletter; please consider subscribing.
Researchers Kalyani Chaubey et al. recently discovered that the drug P7C3-A20 is able to reverse the brain pathology and cognitive decline of advanced Alzheimer’s disease in mice. Alzheimer’s is the most common type of dementia and is considered irreversible, with current therapies offering limited benefit to patients. P7C3-A20 is a compound that improves neuroplasticity and the brain’s response to disease. In the study, published in Cell Reports Medicine, the researchers administered the drug P7C3-A20 to mice with mid-disease stage Alzheimer’s, the stage in which cognitive impairment emerges, and to mice with advanced stages of Alzheimer’s. For the mid-stage disease mice, P7C3-A20 prevented memory impairment.
Even more notably, in the severe-stage mice, the P7C3-A20 intervention resulted in full cognitive recovery, reduction or reversal of neuropathologies, and “comprehensively restored brain health and function by 12 months.” Dr. Pieper, a senior author of the study, commented, “The key takeaway is a message of hope—the effects of Alzheimer's disease may not be inevitably permanent… The damaged brain can, under some conditions, repair itself and regain function.”
Nicotinamide adenine dinucleotide (NAD+) homeostasis—the balance of NAD+ molecules in the brain—is incredibly important for cellular resistance against numerous brain deteriorations, including DNA damage and neurodegeneration. NAD+ molecules are critical for maintaining the brain’s ability to recover from damage. While NAD+ homeostasis naturally declines with age, the researchers found NAD+ dysregulation correlates with the severity of Alzheimer’s Disease. In the study, the mice bred to develop Alzheimer’s exhibited a 30% reduction in NAD+ homeostasis 6 months into their disease. However, with the P7C3-A20 intervention, their NAD+ homeostasis was restored, which was associated with the reversal of memory and cognitive deficits that had previously been observed.
Along with these results, blood levels of phosphorylated tau 217, a biomarker associated with neurodegeneration similar to that typical of Alzheimer’s, returned to normal levels after the administration of P7C3-A20. The authors note that in humans with Alzheimer’s, there is also decline in NAD+ homeostasis that is correlated with Alzheimer’s pathologies. This study provides a much more hopeful view of Alzheimer’s and neurodegeneration in general, though more research is needed before a medication can be developed for humans.
