Neurofibrillary changes following childhood lead encephalopathy.
This report details the findings in a patient who survived severe lead encephalopathy at age 2 1/4 years, to die 42 years later in a state of severe mental deterioration. The brain revealed diffuse cortical atrophy, most severe in the temporal lobes, followed by hippocampi, amygdaloid nuclei and frontal cortex. Numerous pyramidal cells of the forebrain grisea contained Alzheimer's neurofibrillary tangles. The remaining pyramidal cells of the hippocampi exhibited granulo-vacuolar degeneration. Many senile plaques were present predominantly in the atrophic temporal cortex. Electron microscopic examination revealed many 800 A twisted tubules in the tangles. Atomic absorption spectrophotometry disclosed a tenfold increase of lead in frontal and temporal cortices as compared to suitable controls. The possibility that toxic levels of lead in any form could result in the formation of Alzheimer's fibrillary tangles is discussed.
D000328:Adult; D000535:Aluminum / Q000032:analysis; D000544:Alzheimer Disease / Q000473:pathology; D000679:Amygdala / Q000473:pathology; D000818:Animals; D001921:Brain / Q000473:pathology* / Q000648:ultrastructure; D001923:Brain Chemistry; D002531:Cerebellum / Q000473:pathology; D002540:Cerebral Cortex / Q000473:pathology; D006624:Hippocampus / Q000473:pathology; D006801:Humans; D007854:Lead / Q000032:analysis; D007855:Lead Poisoning / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009454:Neurofibrils / Q000648:ultrastructure*; D011817:Rabbits; D012598:Sclerosis
D007854:Lead; D000535:Aluminum