Alzheimer’s disease: Aluminum and fibrinous proteins

Abstract

Although aluminum is one of the most common elements in the biosphere, no normal functions or biochemical reactions are known for this metal. In chemical reactions, the small ionic radius and high charge (r=.51A; charge=3+) results in prolonged dissociation times compared to other biological cations and probably renders aluminum unsuitable or toxic to many biological systems. Nevertheless, many biological organisms have probably evolved in the presence of considerable concentrations of bioavailable aluminum and appear to have developed either a tolerance or an effective mechanism for exclusion of aluminum from intracellular reactions. Healthy mammalian brain, for instance, appears to have a well regulated aluminum content ranging between 1.1 and 1.9 µg/g dry weight [1]. Mammalian brain possesses a highly effective membrane barrier at the blood-brain interface. In addition, the brain of some species i.e. rats, mice and the neurologically normal human appear to be able to tolerate considerably higher concentrations of intracellular aluminum than species such as the cat and rabbit. In an aluminum sensitive species mean brain tissue concentrations of 6 to 8 µg/g dry weight are lethal [2, 3]. The species variation in the neurotoxic threshold to aluminum support the hypothesis that the brain of certain species have ligands of high aluminum affinity capable of either detoxifying or partitioning the element into biologically unreactive complexes.