New Research Links NAD Balance to Reversal of Alzheimer’s Pathology and Full Cognitive Recovery in Animal Models
Findings reinforce the importance of NAD balance in brain health and the growing relevance of accurate NAD measurement
Groundbreaking research published in Cell Reports Medicine* suggests that restoring NAD (Nicotinamide Adenine Dinucleotide) levels is central to cellular energy and repair and may not only help prevent or slow Alzheimer’s disease but also enable the reversal of disease-related pathology and restoration of cognitive function. The findings from the research in animal models underscore the critical role NAD biology plays in brain health.
For decades, Alzheimer’s disease (AD) has been considered irreversible. However, the new research suggests that disruption of NAD balance is a significant driver of disease progression. Without proper NAD levels, cells lose the ability to perform essential processes required for normal function and survival. The study shows this decline is especially severe in the brains of people with Alzheimer’s, a pattern also seen in mouse models of the disease.
To investigate this further, researchers used genetically engineered mice that replicate key aspects of human Alzheimer’s. One model carried human mutations affecting amyloid processing, while another carried a mutation in the tau protein, two key drivers of early AD pathology. Both developed extensive Alzheimer’s-like brain damage, including neuroinflammation, blood–brain barrier breakdown, axonal degeneration, impaired neurogenesis, reduced synaptic transmission, oxidative damage, and severe cognitive decline.
After confirming that brain NAD levels dropped sharply in both human Alzheimer’s tissue and the mouse models, scientists tested whether maintaining NAD balance before disease onset could prevent pathology, and whether restoring NAD balance after significant disease progression could enable recovery.
Remarkably, preserving NAD balance protected mice from developing Alzheimer’s-like disease. Even more notably, delayed treatment in mice with advanced pathology reversed major disease processes and restored cognitive function in both amyloid- and tau-driven models. While Alzheimer’s remains a uniquely human condition and clinical trials are still required, these findings mark an important shift in how researchers understand neurodegeneration, ageing, and cellular resilience.
NADs are coenzymes found in every living cell and are essential for energy production, mitochondrial function, DNA repair, and cellular maintenance, helping protect cells against age-related stress. As people age, NAD levels can decline, and in Alzheimer’s pathology, this decline is significantly more pronounced, leaving brain cells increasingly unable to maintain function or repair damage.
The Need for Accurate Testing
With Alzheimer’s risk significantly higher among individuals with a family history of the disease, the findings also highlight the potential value of early, preventive action. Monitoring NAD levels before cognitive symptoms appear may provide insight into cellular and metabolic health at a stage when intervention could be most effective.
Despite its growing relevance, NAD is not routinely measured. Millions of adults take a various NAD precursors and supplements without knowing whether their NAD levels are actually improving. Without personalised biological data, individuals may be making health decisions without understanding their cellular status.
NADMED has developed the world’s only CE-marked blood test for measuring NAD levels, offering a fast, validated, and accurate method to quantify both NAD⁺ and NADH, enabling evidence-based decisions around clinical setting, supplementation, nutrition, longevity strategies, and metabolic wellbeing.
Jari Närhi, CEO of NADMED, commented, “NAD biology is becoming central to how we understand ageing and brain health. This research reinforces an important principle: without measuring NAD levels, it’s difficult to make informed decisions about prevention or optimisation. Accurate measurement supports a shift from assumption to evidence in personalised health.”
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