Coexistence of reactive plasticity and neurodegeneration in Alzheimer diseased brains

• J. Guevara ^[1] ; H. Dilhuydy ^[3] ; B. Espinosa ^[4] ; A. Delacourte ^[5] ; R. Quirion ^[2] ; R. Mena ^[6] ; Y. Joanette ^[3] ; E. Zenteno ^[7] ; Y. Robitaille ^[3]
  1. [1] Instituto Nacional de Neurología y Neurocirugía

     Instituto Nacional de Neurología y Neurocirugía

     México

     
  2. [2] McGill University

     McGill University

     Canadá

     
  3. [3] Institut Universitaire de Gériatrie de Montréal, Canada
  4. [4] Departamento de Bioquímica, Mexico, DF
  5. [5] Neuroendocrinologie et Physiopathologie Neuronale. Unité INSERM 422, Lille, France
  6. [6] CINVESTAV, Mexico, DF
  7. [7] UNAM, Mexico, DF

  Mostrar afiliaciones +
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 19, Nº. 4, 2004, págs. 1075-1084
• Idioma: inglés
• Enlaces
  • Texto completo
• Resumen

  • Alzheimer’s disease (AD) is a pathological process characterized by neuron degeneration and, as recently suggested, brain plasticity. In this work, we compared the reactive plasticity in AD brains associated to O-glycosydically linked glycans, recognized by lectins from Amaranthus leucocarpus (ALL) and Macrobrachium rosenbergii (MRL), and the tau neuritic degeneration. The neuritic degenerative process was evaluated by the quantification of aggregated neuritic structures. Lesions were determined using antibodies against hyperphosphorylated-tau (AD2), amyloid-ß, and synaptophysin. In these conditions, we classified and quantified three pathological structures associated to the neuritic degenerative process: 1) Amyloid-ß deposits (AßDs), 2) Classic neuritic plaques (NPs), and 3) Dystrophic neurites clusters (DNCs) lacking amyloid-ß deposits. Reactive plasticity structures were constituted by meganeuritic clusters (MCs) and peri-neuronal sprouting in neurons of the CA4 region of the hippocampus, immunoreactive to synaptophysin (exclusively in AD brains) and GAP-43. Besides, MCs were associated to sialylated O-glycosydically linked glycans as determined by positive labeling with ALL and MRL. Considering that these lectins are specific for the synaptic sprouting process in AD, our results suggest the co-occurrence of of several areas of reactive plasticity and neuron degeneration in AD.