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Nicotinamide adenine dinucleotide (NAD+) may be one of the most overlooked factors when it comes to optimizing cellular health. It is a cellular coenzyme that plays a role in many metabolic and signaling reactions.

For example, it partakes in redox reactions —chemical exchanges that transfer energy between molecules— which lead to the production of adenosine triphosphate (ATP), your body’s energy currency.1In fact, research shows that a deficiency is linked to an array of conditions, such as sarcopenia and diabetes.2

But that’s not all — Alzheimer’s disease, the most common form of dementia,3has now been linked to declining NAD+ levels. Following this line of thought, emerging research shows that boosting NAD+ intake can reverse the progression of Alzheimer’s disease. This discovery could be one of the biggest breakthroughs in recent times, as most people believe that Alzheimer’s only worsens the longer it goes,4and treatment focuses on slowing decline rather than reversing it.

A study published in Cell Reports Medicine set out to discover how Alzheimer’s disease can be reversed by boosting NAD+ levels. For the experiment, the researchers used multiple mouse models of Alzheimer’s disease that already showed severe cognitive impairment, brain inflammation, tau pathology, and structural brain damage.5

Mice were administered P7C3-A20 at a dosage of 10 milligrams (mg) per kilogram (kg) of weight each day. Analysis involved observing changes across behavior, brain chemistry, and physical brain structure. For context, P7C3-A20 is a carbazole compound that can readily cross the blood-brain barrier. It works by binding to NAMPT (an enzyme that controls how much NAD+ is made from niacinamide) to enhance NAD+ production6at safe levels.

•One striking finding is the rate of improvement —The authors reported that in treated mice, cognitive function recovered fully, meaning their memory performance returned to levels seen in healthy animals. These mice performed just as well as non-diseased controls on learning and memory tests.

•What changed inside the brain samples —Multiple hallmarks of Alzheimer’s disease improved at the same time. Tau pathology, which refers to tangled protein structures that disrupt neuron function, decreased after NAD+ restoration. Neuroinflammation markers dropped, indicating a calmer immune environment in the brain. Signals of oxidative stress and DNA damage — both signs of energy failure inside cells — also declined.

•Results were observed right away —The intervention occurred after the disease had fully developed in these animals. Again, this directly challenges the long-standing belief that Alzheimer’s damage becomes permanent once it crosses a certain threshold.

•Other disease models were used to solidify the findings —The researchers tested the same approach in two different forms of Alzheimer’s pathology. In amyloid-driven mice and in tau-driven PS19 mice, restoring NAD+ reversed advanced disease features. That distinction matters because amyloid and tau represent different biological drivers of Alzheimer’s. Seeing improvement in both strengthens the argument that NAD+ disruption sits upstream of these visible brain lesions.

Source: SGT Report