Researchers at University Hospitals and Case Western Reserve University report that restoring NAD enzyme activity reversed multiple brain pathologies and fully recovered cognitive performance in mice engineered to carry human Alzheimer’s genes. The team used a novel compound to restore NAD function and validated effects with behavioral learning and memory tests. Investigators caution these are preclinical results and human trials are still years away, while recommending healthy sleep, diet and cognitive activity to help reduce risk.
University Hospitals Study Reverses Alzheimer’s Signs In Mice, But Human Trials Are Years Away
University Hospitals researchers hope new study is first step in reversing Alzheimer’s
A diagnosis of Alzheimer’s disease profoundly alters lives as brain function slowly declines and ultimately fails to support normal cognition and independence.
Researchers at University Hospitals, in collaboration with Case Western Reserve University, report a preclinical study they say is an initial step toward reversing some effects of the disease. The project grew out of earlier work on one major Alzheimer’s risk factor: traumatic brain injury.
Dr. Andrew Pieper, professor of psychiatry and neurosciences at Case Western Reserve University and University Hospitals, said the team focused on enzymes that depend on nicotinamide adenine dinucleotide (NAD). NAD-dependent enzymes exist in every living cell and help maintain the cellular energy needed for repair processes. In people with Alzheimer’s, the activity of these enzymes declines.
To test whether restoring NAD function could alter disease course, researchers introduced human genes linked to Alzheimer’s into mice to create an animal model of the illness. After the mice developed Alzheimer-like pathology, the team administered a compound they developed to restore NAD enzyme activity.
When we decoded it at the end, we were just thrilled to see that across the board we had reversed so many different features of pathology in the brain and recovered cognitive function fully — as if the animal never had the disease in the first place, Pieper said.
According to the team, treated animals were assessed with a broad battery of behavioral tests, including learning and memory evaluations, and performed at normal levels after treatment. The investigators describe the work as a proof of principle that some effects of dementia may be reversible in an animal model.
Pieper and colleagues emphasize important caveats: results in mice do not guarantee similar outcomes in humans, and the path to clinical trials will take years of additional research and safety testing. The compound and approach remain at the preclinical stage while researchers continue to analyze data and plan further studies.
Meanwhile, the team recommends proven risk-reduction measures: prioritizing good sleep, a balanced diet, regular physical activity, and mentally stimulating pursuits to help lower Alzheimer’s risk.
Note: This report summarizes preclinical research in mice. It does not indicate an available treatment for people at this time.
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