The Company's first discovery was a patented method of treating the earliest components of brain damage in Parkinson's Disease, Alzheimer's Disease, and Lou Gehrig's Disease by preventing mitochondrial DNA damage.
The fundamental achievement of the Company's research is to prevent and control damage to mitochondria, which are comparable to powerhouses. Subsequently the strategy assists brain cells in repair by increasing the levels of growth factors. However the growth factors would not have effect if the mitochondria had not been protected from damage.
Verne Mendel’s primary neuroprotection technology is a unique method of preventing mitochondrial damage and inducing repair in the nervous system. It has been extended to demonstrate effect in other neurotoxic and metabolic toxin disease models.
This method of preventing neurotoxic damage also leads to a means to prevent eta amyloid deposition by inhibiting enzymatic activity at the Beta secretase site. The Company has identified enzymes capable of cleaving the amyloid precursor protein into eta amyloid. Thus Alzheimer’s disease may be treated in a novel manner.
Goals of Treatment:
The technology provides the following treatment opportunities:
In Parkinson’s, Alzheimer’s and Lou Gehrig’s Diseases treatment addresses the major components of disease including mitochondrial DNA damage, growth factor gene expression, receptor regulation, energetics and redox homeostasis and beta amyloid production.
In Stroke treatmetn can control the mitochondrial DNA damage, growth factor deficiency and ATP deficiency during the ischemic reperfusion period post stroke.
In Diabetes treatment can prevent the mitochondrial DNA damage, ATP loss, failure of exocytosis of insulin, it can enhances glucose uptake and insulin sensitivity, thus preventing the vascular complications of the disease.
In Atherosclerosis and Cardiomyopathy treatment can prevent the mitochondrial DNA damage and maintain production of the energy compound ATP.
In Glaucoma treatment can prevent mitochondrial DNA damage and excititoxic damage in retinal ganglion cells.
In Presbycusis (sensorneural deafness) treatment can prevent cochlear mitochondrial DNA damage.
In Neuropathy treatment can prevent mitochondrial DNA damage and maintain ATP production.