New Delhi, Dec 25 (NationPress) In a groundbreaking discovery, researchers from the United States have demonstrated through animal studies that Alzheimer's disease may actually be reversible, which contradicts over a century of research that deemed this neurodegenerative condition irreversible.

The findings, published in the journal Cell Reports Medicine, utilized various preclinical mouse models alongside human Alzheimer's brain samples, highlighting that maintaining an optimal NAD+ balance can not only prevent but also reverse the progression of the disease.

NAD+ serves as a crucial cellular energy molecule and is a significant contributor to the development of Alzheimer's.

The research team further established that the reduction in NAD+ levels is notably more pronounced in the brains of individuals suffering from Alzheimer's, a trend that was also observed in the corresponding mouse models.

“We were incredibly excited and motivated by our findings,” stated Andrew A. Pieper, the senior author of the study and Director of the Brain Health Medicines Center at the Harrington Discovery Institute, University Hospitals.

“Restoring the brain's energy equilibrium led to both pathological and functional recovery in two distinct mouse lines afflicted with advanced Alzheimer's. Observing this positive outcome in two genetically diverse animal models reinforces the notion that reinstating the brain's NAD+ balance could aid in the recovery of Alzheimer’s patients,” he elaborated.

The research focused on mice genetically modified to express mutations that lead to Alzheimer's in humans. The team utilized two specific models for their experiments.

One mouse line possessed multiple human mutations related to amyloid processing, while the other showcased a mutation in the tau protein.

Upon discovering that NAD+ levels in the brain drastically declined in both human and mouse subjects with Alzheimer's, the researchers explored whether maintaining NAD+ levels prior to disease onset or restoring them after significant disease progression could either prevent or reverse Alzheimer's.

They achieved the restoration of NAD+ balance through the administration of a well-characterized pharmacological agent known as P7C3-A20.

Astonishingly, not only did preserving NAD+ balance shield mice from developing Alzheimer's, but also, delayed treatment in mice with advanced disease facilitated the brain's ability to rectify major pathological events caused by genetic mutations. Furthermore, both lines of mice completely regained their cognitive functions.