Intraventricular administration of the cholinotoxin AF64A increases the accumulation of aluminum in the rat parietal cortex and hippocampus, but not in the frontal cortex.

Aluminum (Al) concentrations of the rat frontal cortex, parietal cortex, and hippocampus were measured by atomic absorption spectroscopy 16 days after a unilateral intracerebroventricular injection of Na gluconate, Al gluconate, or the cholinotoxin AF64A. A fourth group of rats were injected with AF64A 6 days before injection of Al gluconate and subsequently sacrificed 10 days later. The combined treatment of AF64A and Al gluconate resulted in enhanced intraneuronal accumulation of Al in the parietal cortex and hippocampus but not in the frontal cortex. Consequently, Al may not be considered to be a primary factor in the pathogenesis of Alzheimer's disease.