Coexistence of reactive plasticity and neurodegeneration in Alzheimer diseased brains
J. Guevara1, H. Dilhuydy2, B. Espinosa3, A. Delacourte4, R. Quirion5, R. Mena6, Y. Joanette2, E. Zenteno7 and Y. Robitaille2
1Laboratorio de Enfermedades Neurodegenerativas. Instituto Nacional de Neurología y Neurocirugía, Mexico, DF, 2Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, Canada, 3Departamento de Bioquímica, Mexico, DF, 4Neuroendocrinologie et Physiopathologie Neuronale. Unité INSERM 422, Lille, France, 5Douglas Hospital Research Center, McGill University, Verdun, Quebec, Canada, 6Departamento de Neurociencias, CINVESTAV, Mexico, DF and 7Departamento de Bioquímica, Facultad de Medicina, UNAM, Mexico, DF
Offprint requests to: Jorge Guevara, Laboratorio de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía, Insurgentes Sur 3877. Col. La Fama. Del. Tlalpan, 14269 México DF, México. Fax: (52) 55 54 24 08 08. e-mail: jguevara@innn.edu.mx
Summary. 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. Histol Histopathol 19, 1075-1084 (2004)
Key words: Alzheimer’s disease, Amyloid-ß, Tau, Brain plasticity, ApoE
DOI: 10.14670/HH-19.1075