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.

Alzheimer Disease↗

PubMedDate not supplied

Alzheimer's disease: paired helical filaments and cytomembranes.

Observations were made with the electron microscope on biopsies from the frontal cerebral cortex of four patients showing the clinical symptoms of advanced Alzheimer's disease (AD). Sections from all four biopsies showed neuronal dendrites, and to a lesser extent, perikarya, packed with paired helical filaments (PHFs) and a correlated complete loss of the normal content of microtubules. It was usually impossible to visualize the beginning and end of the PHF since it passed out of the plane of section. However, not infrequently, PHFs could be seen apparently arising at or from the surfaces of cytomembranes. Such membranes (in perikarya or dendrite) often formed irregular stacks or lamellated bodies. These membranes were invariably agranular (i.e. not studded with ribosomes) and so might be considered as pathological forms of smooth endoplasmic reticulum (SER). A correlation is established between the known biochemical nature of PHFs and their postulated membrane origin.

Alzheimer Disease↗

PubMedDate not supplied

Dendritic inclusions in the cerebellar granular layer after long term alcohol consumption in adult rats.

Whorled multiplanal inclusions up to 1.5 micron in diameter were observed in dendrites of the cerebellar Golgi cells after 6 months of alcohol treatment, increasing in number with time. Inclusions are formed by apposed cytomembranes stacked parallel or in a twisted arrangement. The paired membranes merged into a dense, finely textured material. A close relationship with dendritic smooth endoplasmic reticulum is apparent. A correlation between chronic alcohol intake and the development of these inclusions is shown although, in common with many other types of neuronal cytoplasmic inclusions, their genesis and function remains to be determined.

Alcoholism↗

PubMedDate not supplied

Survival skills: a patient teaching model for diabetes mellitus.

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Diabetes Mellitus↗