A New Approach

In the last decade, efforts to develop disease modifying therapies have been focused primarily on amyloid beta and tau aggregation hypotheses. There have also been efforts evaluating neuroprotective mechanism as potential therapeutic approaches. Drug development to address these theories has been disappointing, with few success and many failures. There exists a tremendous need for innovative and alternative AD therapies.



Deficient Glucose Metabolism

The brain is one of the most metabolically active organs in the body and under normal conditions it relies primarily on large amounts of glucose for its energy needs. Research findings have shown that AD patients have lower levels of brain glucose metabolism. In these studies, this lower brain glucose metabolism correlated with worsening performance on memory tests. Subsequent studies have demonstrated that reduced glucose metabolism occurs early in the disease process and worsens as the disease progresses.



A New Energy

Addressing Deficient Glucose Metabolism

During times of low glucose availability, such as fasting, ketones are the brain’s natural back-up fuel, available for use by neurons as an alternative source of energy. Inside these neurons, ketones can be used by the mitochondria instead of glucose to produce the cellular energy needed to power basic cellular function and synaptic activity. Ketones can provide up to 60% of the brains energy needs when glucose is unavailable. Ketones also act as signaling molecules that confer stress resistance and ant-inflammatory properties.




Our Mechanism of Action