Progression of Alzheimer histopathological changes.
The clinical-pathological correlations that were prospectively obtained in a cohort of old patients (> 75 years of age) are reviewed. The pathological data were obtained in 31 cases, either normal or affected by Alzheimer disease of various degrees of severity. The density of the A beta peptide deposits was poorly linked with the intellectual status. One patient had a very high density of deposits, although she was considered intellectually normal. When present in a patient, the A beta deposits usually involved all the cortical samples; the samples devoid of deposits most often belonged to the limbic system. The distribution of the neurofibrillary tangles was highly selective: the primary areas (such as the visual cortex) were lesioned only in a few cases, invariably the most severely affected ones. Neurofibrillary tangles involved the associative cortices (sparing the primary areas) in the cases of intermediate severity. The hippocampal-parahippocampal areas contained at least a few neurofibrillary tangles in all the cases. The prevalence of the neurofibrillary lesions in that cohort of cases probably indicated the chronological (and hierarchical) order of involvement: from limbic to associative, from associative to primary areas. There was a linear relationship between the density of the neurofibrillary tangles and the intellectual deficit in the hippocampal-parahippocampal gyrus. The relationship was stepwise rather than linear in the isocortical samples, suggesting that the neurofibrillary tangles were a late phenomenon in those types of cortices. An accumulation of SNAP 25 immunoreactivity was found in some of the most severely affected cases, pointing to a deficit in axonal transport. The density and the total number of neurons were evaluated in a sample of the supramarginal gyrus. The neuronal loss was found to be severe, but only in the most affected cases, when the density of neurofibrillary tangles was higher than 5/mm2.
Laboratoire de Neuropathologie R. Escourolle, Paris, France.
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Duyckaerts
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MA
Colle
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Dessi
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F
Piette
J J
JJ
Hauw
D000368:Aged; D000544:Alzheimer Disease / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000032:analysis; D018450:Disease Progression; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D009419:Nerve Tissue Proteins / Q000032:analysis; D011446:Prospective Studies; D016875:tau Proteins / Q000032:analysis
D016229:Amyloid beta-Peptides; D009419:Nerve Tissue Proteins; D016875:tau Proteins