ChromaDex Corp. reported in the peer-reviewed journal Translational Neurodegeneration by a team of scientists led by Dr. Adil Mardinoglu, Professor of Systems Biology in the Science for Life Laboratory at the Royal Institute of Technology (KTH), Stockholm, Sweden ??and Centre for Host-Microbiome Interaction at the King's College London, UK. The clinical trial was part of the ChromaDex External Research Program (CERP™) and investigated a combined metabolic activator (CMA), or ingredient ‘cocktail', featuring the company's proprietary Niagen® ingredient (patented nicotinamide riboside or NR) in addition to L-carnitine tartrate, serine, and N-acetyl-L-cysteine (NAC) in 60 mild-to-moderate patients with Alzhemer's disease (AD).

Results demonstrated CMA supplementation significantly improved cognitive function by 29% (vs. only 14% in the Placebo group) and markers of liver and kidney health in AD patients compared to Placebo after 84 days of supplementation. This study marks a milestone as it is the first-ever peer-reviewed clinical study to investigate the effects of CMA supplementation in human AD patients.

The use of this CMA builds on previous successful clinical and preclinical studies, which demonstrated CMA effectiveness. In a preclinical study, AD and Parkinson's disease (PD) rat models were used to demonstrate CMA supplementation resulted in improved brain and liver metabolism. Further, results revealed that hyperemia (blood flow), degeneration (loss of nerve structure or function) and necrosis (death of neurons) in brain neurons were improved by CMA administration in both AD and PD animal models (Science Direct).

In two earlier human clinical trials, CMA supplementation improved liver health in patients with nonalcoholic fatty liver disease (NAFLD) and improved recovery time of patients with COVID-19 (Molecular Systems Biology; Advanced Science). In both clinical trials, the success of the CMA was partly attributed to its beneficial effect on mitochondrial health and function. Several risk factors are associated with AD including age, poor lifestyle, genetic mutations, and metabolic dysfunction.

Although the exact mechanism of the development of AD remains unknown, a large body of evidence suggests that dysfunctional mitochondria and brain energy metabolism may play key roles in its development. Because mitochondria are critical for cellular energy production, significant changes in mitochondrial function are linked to energy failure and brain cell death. In fact, research suggests optimal mitochondrial health not only helps support brain cell activity by providing cells with sufficient energy, but also protects them by mitigating oxidative stress (a disturbance in the balance between the production of reactive oxygen species, or free radicals, and antioxidant defenses) and damage.

Therefore, Dr. Adil Mardinoglu's team sought to determine if supporting mitochondrial function may be an effective strategy in helping improve the symptoms observed in AD patients.