Scientists from Case Western Reserve University (CWRU), University Hospitals, and the Louis Stokes Cleveland VA Medical Center have made significant strides in Alzheimer’s research, suggesting that recovery from this devastating disease may be possible. A recent study revealed that a compound known as P7C3-A20 was effective in preventing Alzheimer’s disease in lab mice and even reversing cognitive decline in those with advanced stages of the illness.
In the study, the researchers looked at P7C3-A20, a neuroprotective compound that was injected into lab mice genetically modified to develop Alzheimer’s. These mice have been engineered to develop mutations in either amyloid or tau proteins. These mice were treated at 2 months of age, which was done in time to completely protect them from ever developing the disease. This encouraging result shows that early intervention with P7C3-A20 may have an important role in preventing Alzheimer’s.
In addition, the research proved that P7C3-A20 was equally effective for laboratory mice afflicted with severe Alzheimer’s disease. Once injected at six months of age, these mice had notably partial cognitive rescue following treatment. Finding a way to restore NAD+ levels back to baseline was the other huge breakthrough. This discovery underscores the important role that the compound plays in preserving brain health.
Andrew A. Pieper, a CWRU professor of neuroscience and the study’s principal investigator. He understood how to explain what the findings meant to best convince people to act.
“Restoring the brain’s energy balance achieved pathological and functional recovery in both lines of mice with advanced Alzheimer’s. Seeing this effect in two very different animal models, each driven by different genetic causes, strengthens the new idea that recovery from advanced disease might be possible in people with AD when the brain’s NAD+ balance is restored.” – Andrew A. Pieper
To evaluate the efficacy of P7C3-A20, the researchers used two different animal models. This original model went on to develop Alzheimer’s because of a defined mutation in the amyloid protein. By contrast, the second model bore a mutation linked to tau protein. Of these, P7C3-A20 has exhibited extraordinary promise in preventing Alzheimer’s in both models. This outcome demonstrates the compound’s versatility and potency at being effective towards all three genetic causes/triggers of the disease.
The study’s results present a significant leap forward in understanding how alterations in brain chemistry can influence Alzheimer’s progression and recovery. In advanced cases of Alzheimer’s disease, restoring NAD+ is vital to reversing cognitive decline. This seemingly ordinary molecule, known as acetyl-CoA, is a linchpin of energy metabolism in nearly all of our cells.
Pieper went on to stress the larger relevance of this research to human health.
“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.” – Andrew A. Pieper
These new discoveries may pave the way for future clinical trials. They hope to convert this animal research towards developing actual treatments for humans fighting the effects of Alzheimer’s disease. Yet the journey from promising laboratory results to a reality in patient care is often long, complex, and fraught with challenges. The prospect of being able to restore cognitive function provides new hope to families suffering from this devastating disease.
