作者: M. J. de Leon , G. Smith , A. E. George , T. McRae , J. Golomb
DOI: 10.1007/978-1-4684-6805-2_19
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摘要: Postmortem studies reveal numerous biochemical and neurotransmitter deficits in Alzheimer’s disease (AD) patients relative to elderly controls. Many of these are more pronounced the hippocampus; than neocortex (for a review see Selkoe Kosik, 1983). There many structural hippocampal abnormalities documented AD. They include neuronal loss, granulovacuolar degeneration, neurofibrillary tangles, neuritic plaques (Kemper, 1984). In AD neuropathological findings show consistent topography with respect formation its projections. Pyramidal cells primary population involved. These affected located within entorhinal cortex (the neurons origin perforant pathway), subiculum, CA1 hippocampus, temporal association cortex. This pattern degeneration results “isolation” from neocortical areas (Hyman et al.,