AXONA^® IS A NOVEL METABOLIC APPROACH TO ALZHEIMER’S DISEASE

The normal/healthy brain depends on circulating glucose for most of its functions.

In Alzheimer’s disease, glucose is poorly utilized by neurons; glucose hypometabolism can lead to low ATP levels and loss of synaptic function.

Axona bypasses defective glucose handling^1-3

Axona is digested and metabolized by the liver to form ketone bodies. Ketone bodies are used by the brain and provide an alternative energy source to neurons with compromised glucose metabolism. Neurons can utilize ketone bodies even in the presence of glucose.

To further explore the merits of hypometabolism therapy with Axona, download the folowing publication.

References: 1. Axona [Prescribing Information]. Broomfield, CO: Accera, Inc.; September 2009. 2. Henderson ST, Vogel JL, Barr LJ, et al. Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer’s disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutr Metab (Lond). 2009;6:31. 3. Costantini LC, Barr LJ, Vogel JL, Henderson ST. Hypometabolism as a therapeutic target in Alzheimer’s disease. BMC Neurosci. 2008;9(Suppl 2):S16.