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About 5.2 million Americans have Alzheimer's disease. The underlying cause of this disease is not fully understood and current treatments are only moderately effective, leaving millions without hope of meaningful improvement.
Axona, a medical food designed for the clinical dietary management of the metabolic processes associated with mild-to-moderate Alzheimer's disease, represents a novel therapeutic option.
Research has expanded our knowledge of disease biology, resulting in new, therapeutic strategies.
The development of Axona leverages findings about glucose hypo-metabolism and its role in Alzheimer's.
The human brain is one of the most metabolically active organs in the body. Under normal conditions, it relies almost exclusively on glucose for fuel.
Glucose is transported across the blood-brain barrier into cells by specialized facilitative transporter proteins.
Most of the glucose absorbed is oxidatively metabolized for Adenosine-Triphosphate, or ATP, synthesis. This fuels basic cellular functions and synaptic activity.
A prominent and well-characterized feature of Alzheimer's disease is a progressive region-specific decline in cerebral glucose metabolism. Glucose hypo-metabolism can lead to low ATP levels and loss of synaptic function.
Although the brain cannot use most of the usual alternative energy sources, it can use ketone bodies. Therapeutic agents that are metabolized to form ketone bodies can enhance ketone-body blood-levels.
Axona is absorbed from the gastro-intestinal tract after oral administration and is metabolized by the liver into ketone bodies, which are released into the bloodstream for use by brain cells.
Ketone bodies can provide up to 60% of the energy requirements of neurons.
Ketone bodies leave the circulation, cross the blood-brain barrier, and enter the neuron, where they are metabolized, to provide energy.
Ketone bodies can provide up to 60% of the energy requirements of neurons, even if glucose is present.
Beta-Hyroxybutyrate (BHB) is a ketone body. Only three metabolic steps are required to metabolize BHB into acetyl-CoA, which enters the citric acid cycle, culminating in ATP production.
Nerve impulses can now be successfully transmitted across the synapse, illustrating that a ketone-body-derived energy source can return the hypo-metabolic neurons to a functional state.
Discover Axona, a medical food intended for the clinical dietary management of the metabolic processes associated with mild-to-moderate Alzheimer's disease. Axona is medical-food for thought.
Axona is a brand new medical food for treating Alzheimer's, which is the most common form of dementia. It is regulated by the FDA. Axona works by providing an alternative energy source for brain cells.
A new Northwestern University study found that as we age, the brain may not get enough glucose (sugar, which is the brain's main source of energy). This launches a process producing sticky clumps of protein that appear to be a cause of Alzheimer's.
The development of Axona leverages findings about glucose hypo-metabolism and its role in Alzheimer's.
The human brain is one of the most metabolically active organs in the body. Under normal conditions, it relies almost exclusively on glucose for fuel.
Glucose is transported across the blood-brain barrier into cells by specialized facilitative transporter proteins.
Most of the glucose absorbed is oxidatively metabolized for Adenosine-Triphosphate, or ATP, synthesis. This fuels basic cellular functions and synaptic activity.
A prominent and well-characterized feature of Alzheimer's disease is a progressive region-specific decline in cerebral glucose metabolism. Glucose hypo-metabolism can lead to low ATP levels and loss of synaptic function.
Nerve impulses can now be successfully transmitted across the synapse, illustrating that a ketone-body-derived energy source can return the hypo-metabolic neurons to a functional state.
