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CT, MRI, and PET Studies of Hippocampal Pathology in Alzheimer’s Disease

  • M. J. de Leon
  • G. Smith
  • A. E. George
  • T. McRae
  • J. Golomb
  • A. Convit
  • A. Kluger
  • W. Tsui
  • S. H. Ferris
  • A. P. Wolf

Abstract

Postmortem studies reveal numerous biochemical and neurotransmitter deficits in Alzheimer’s disease (AD) patients relative to elderly controls. Many of these deficits are more pronounced in the hippocampus; than in the neocortex (for a review see Selkoe and Kosik, 1983). There are many structural hippocampal abnormalities documented in AD. They include neuronal loss, granulovacuolar degeneration, neurofibrillary tangles, and neuritic plaques (Kemper, 1984). In AD these neuropathological findings show a consistent topography with respect to the hippocampal formation and its projections. Pyramidal cells are the primary neuronal population involved. These affected cells are located within the entorhinal cortex (the neurons of origin of the perforant pathway), the subiculum, CA1 of the hippocampus, and the temporal association cortex. This pattern of degeneration results in the “isolation” of the hippocampal formation from its neocortical association areas (Hyman et al., 1984).

Keywords

Hippocampal Atrophy Hippocampal Pathology Granulovacuolar Degeneration Hippocampal Fissure Hippocampal Change 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Birkhäuser Boston 1992

Authors and Affiliations

  • M. J. de Leon
  • G. Smith
  • A. E. George
  • T. McRae
  • J. Golomb
  • A. Convit
  • A. Kluger
  • W. Tsui
  • S. H. Ferris
  • A. P. Wolf

There are no affiliations available

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