Recent developments show that the brains of persons who have died from Alzheimer's Disease (AD) have a deficiency of Essential Fatty acids in one of the principal classes of phospholipids. It is hypothesized that faulty brain cell membranes resulting from this deficiency may allow passage of an enzyme into the bilayer membrane space which cuts beta amyloid precursor proteins attached to such cells at a critical intramembrane position releasing a complete sequence of beta amyloid protein into the extracellular space. Beta amyloid protein appears to be the principal active constituent of senile plaques thought to be a probable cause of brain damage resulting in AD.
Treatment of persons suffering from AD with desferrioxamine, a trivalent ion chelator to remove aluminum has shown results in slowing the progression of this disease, implicating aluminum and/or other chelated substances in its etiology. Both EFA deficiency and aluminum buildup may be prevented by dietary precautions.