For decades, Alzheimer’s disease has been treated as a one-way street. Once memory fades and brain damage sets in, the thinking goes, there is no turning back. But a new study published in the journal Cell Reports Medicine delivers a jolt of optimism—showing that advanced Alzheimer’s damage can be reversed in lab animals.
Researchers tested an experimental compound called P7C3-A20 in mice bred to develop severe Alzheimer’s-like disease. These mice already had classic warning signs: toxic amyloid plaques, tangled tau proteins, brain inflammation, leaky blood vessels in the brain, and major memory loss. In short, their disease was well underway.
After treatment, the results were stunning. The mice recovered their ability to learn and remember, essentially returning to normal cognitive function. At the same time, many biological hallmarks of Alzheimer’s went into reverse.
The secret weapon appears to be a molecule called NAD+, which helps cells make energy and repair damage. Healthy brains maintain stable NAD+ levels, but the researchers found that both mice and humans with worse Alzheimer’s pathology showed major disruptions in this system. P7C3-A20 works by restoring NAD+ balance, giving struggling brain cells the support they need to survive.
Once NAD+ levels were corrected, the dominoes began to fall—in a good way. Harmful tau proteins declined, inflammation cooled down, oxidative stress dropped, and DNA damage was reduced. The brain’s protective blood-brain barrier became stronger again. Even more surprising, the treatment kick-started the growth of new neurons in the hippocampus, a region critical for memory, and improved communication between brain cells.
The benefits weren’t limited to one type of Alzheimer’s model. The compound also reversed disease signs in mice driven mainly by tau damage rather than amyloid. In lab experiments, it protected human brain blood vessel cells from stress-related injury. Blood levels of p-tau217—a key biomarker doctors are beginning to use to track Alzheimer’s in people—also fell after treatment.
The researchers went a step further, identifying 46 proteins linked to advanced Alzheimer’s that were “reset” by the drug in mice. Those same proteins are disrupted in human Alzheimer’s brains. Interestingly, people who had Alzheimer’s brain changes but never developed dementia showed gene patterns suggesting their NAD+ systems stayed intact.
This isn’t a cure—and it’s not ready for people yet. Mouse studies don’t always translate to humans. But the message is powerful: Alzheimer’s damage may not be as permanent as once believed. Instead of chasing plaques alone, restoring the brain’s energy and repair systems could open a new path forward.
