BENEFITS OF AXONA

Ketone bodies may play a unique role in improving cognition.

Glucose Hypometablism

Declines in the cerebral metabolic rate of glucose (CMRglc) are a prominent and well characterized feature of Alzheimer’s Disease (AD). Abnormally low rates of CMRglc occur in a characteristic pattern, particularly in the posterior cingulated, parietal, temporal, and prefrontal cortices.

Low CMRglc has been identified early in the disease process, particularly in people at genetic risk of developing AD. The major genetic risk factor for late onset AD is the carriage status of the epsilon 4 variant of the apolipoprotein e gene (E4 carriers). E4 carriers are at increased risk of developing AD and have been shown to have low CMRglc, despite showing no signs of cognitive impairment. This pattern of hypometabolism can be detected in E4 carriers as young as 31 years old, consistent with the notion that AD begins decades before cognitive impairment is evident {Reiman, 2004 #137}.

A means to address hypometabolism involves the induction of ketosis. Ketosis results from the presence of ketone bodies in the blood. Ketone bodies are a normal product of human physiology and are produced by the liver under conditions of low glucose availability, such as during fasting or the use of ketogenic diets. Ketone bodies serve an important function in providing an alternative fuel for the brain during mammalian development and during conditions of low food availability {Owen, 1967 #236}.

This ability to substitute for glucose makes ketone bodies an attractive means to address glucose hypometabolism associated with AD {Prins, 2008 #424} {Henderson, 2008 #495}.

Ketone bodies are rapidly converted to adenosine triphosphate (ATP) and acetylcholine precursors via the tricarboxylic acid (TCA) cycle in the mitochondira of neurons.

 

REFERENCE: Constantini LC, Barr LJ, Vogel JL, Henderson ST. Hypometabolism as a therapeutic target in Alzheimer’s disease. BMC Neurosci. 2008;9(suppl 2):S16