Spongiform encephalopathy: a neurocytologist's viewpoint with a note on Alzheimer's disease.
Ultrastructural studies of spongiform encephalopathy (SE) reveal no very early pathological changes in kuru where membrane lamellation has been reported. This observation is challenged. In the later stages of SE, two main theories are examined--the spiroplasma theory and the prion (6 nm filament) theory. Neither are sufficiently convincing at present. In my own ultrastudies of Creutzfeldt-Jakob disease brain, extensive dismantling of the dendritic microtubule cytoskeleton has been observed. Loss of dendritic cytoskeleton implies loss of dendritic cytotransport with abolition of postsynaptic events. This would explain neurological symptoms and death where other causes, pneumonia etc. are not involved. My experimental model, involving depletion or loss of dendritic microtubules, indicates that spongy vacuoles may be fixation artifacts. In a brief consideration of Alzheimer's disease, loss of dendritic microtubules has also been observed, with the implications mentioned above. Finally, the neuritic plaque will be considered.
D000544:Alzheimer Disease / Q000473:pathology*; D000818:Animals; D001921:Brain / Q000648:ultrastructure*; D001927:Brain Diseases / Q000473:pathology*; D007562:Creutzfeldt-Jakob Syndrome / Q000473:pathology; D003712:Dendrites / Q000648:ultrastructure; D006801:Humans; D007729:Kuru / Q000473:pathology; D051379:Mice; D008854:Microscopy, Electron; D008870:Microtubules / Q000648:ultrastructure; D051381:Rats; D012897:Slow Virus Diseases / Q000473:pathology*; D014617:Vacuoles