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Neurofibrillary degeneration, dendritic dying back, and learning-memory deficits after aluminum administration: Implications for brain aging AbstractIncreased concentrations of aluminum have been observed in the brains of patients with senile dementia and have been implicated in the etiology of that disease. This study assessed the possible behavioral and neurocytologic effects of increased brain aluminum in experimental animals. An infusion of 5 μm aluminum (as aluminum tartrate) was made into the lateral ventricles of young adult male New Zealand white rabbits. On the 10th postoperative day, all animals were trained on a step-down active avoidance task and retested 3 days later. The aluminum-treated rabbits showed deficits on both original learning and retention of this task. Electron microscopic examination of neocortical neurons revealed the presence of 10-nm neurofilamentous tangles in aluminum-treated animals. For analysis of dendritic morphology, layer V pyramidal cells from the sensorimotor cerebral cortex were examined using the Scholl method to determine the number of dendritic branches at 20-μm intervals from the cell body. Although there were no differences in the number of processes leaving the cell body, there was a sharp and progressive decrease in the number of branches with increasing distance from the cell body. This pattern is consistent with that expected from a dying-back process. Experimental Neurology Volume 67, Issue 1, January 1980, Pages 152–162 |
