Preclinical lesions and their progression in the experimental spongiform encephalopathies (kuru and Creutzfeldt-Jakob disease) in primates.
Creutzfeldt-Jakob disease and kuru were studied in experimental primates. Eight animals with clinical disease lasting from 1/2 to 12 1/2 months were evaluated for histological evidence of progression of the pathological triad of neuronal vacuolation, neuronal loss and fibrous astrocytosis. The first change to appear was neuronal vacuolation, in both the body of neurones and in the neuropil. Fibrous astrocytosis was found subsequent to neuronal damage and necrosis. Neuronal loss was apparent when clinical signs were present. As the clinical disease progressed, so did the severity of neuronal loss and astrocytosis. Five animals, 1 1/2-10 1/2 months after intracerebral inoculation, before they had shown any signs of clinical disease, had histological evidence of neuronal vacuolation and astrocytosis.
D000818:Animals; D001253:Astrocytes / Q000473:pathology; D001921:Brain / Q000473:pathology*; D001933:Brain Stem / Q000473:pathology; D002531:Cerebellum / Q000473:pathology; D002540:Cerebral Cortex / Q000473:pathology; D003342:Corpus Striatum / Q000473:pathology; D007562:Creutzfeldt-Jakob Syndrome / Q000473:pathology*; D004195:Disease Models, Animal; D000882:Haplorhini; D006624:Hippocampus / Q000473:pathology; D006801:Humans; D007729:Kuru / Q000473:pathology*; D009474:Neurons / Q000473:pathology; D011323:Primates; D013997:Time Factors