The puzzle of Alzheimer's disease (AD).
A compromised defensive system of brain cells against aluminium, together with local defects in glucose metabolism, causes AD. Lack of citrate is a driving force and free cis-aconitate or glutamate are potential carriers, which enable the exotoxin to cross lipid membranes. Only a few aluminium ions replace magnesium in key positions. They block the reversibility of phosphorylation reactions, which are important for short term memory: sensitization of the insulin receptor and protein phosphorylations. Due to disturbed phosphorylation of the cytoskeleton, protein synthesis runs out of balance. Efforts to restore the disturbed reactions result in AD specific deposits. Aluminium ions are the common cause for the induction of AD pathogenesis in patients with genetic defects, with mechanical brain lesions or with minor infarcts, as well as with changes in the relation between numbers of neurons and neuron nursing glia cells due to age.