Four biopsies of the brain cortex of patients with Alzheimer's disease were used for ultrastructural studies. Three-dimensional reconstruction and morphometric studies of three classical plaques were carried out to determine the distribution of the astrocytes and their processes, and spatial relationships between astrocytes and plaque components. Morphologic and morphometric studies showed marked ultrastructural changes in the astrocytes located in the vicinity of the plaque. Proliferating processes of the two or three astrocytes nearest to the plaque become part of the plaque. Processes of hypertrophic astrocytes touch neighboring vessels, neurons, and amyloid deposits. The volume of the peripheral amyloid deposits in the classical plaques examined exceeds the volume of the amyloid star by about 26%. Amyloid of the classical plaque periphery appears as amyloid wisps. Most amyloid wisps are isolated between astrocytic processes proliferating and penetrating into the plaque. Proliferation and penetration of astrocytic processes into the plaque lead to fragmentation of amyloid deposits and their dispersion. Reduction in the size of amyloid wisps isolated between astrocytic processes toward the plaque periphery and changes in the morphology of amyloid fibers in this plaque region suggest that astrocytes participate in gradual degradation of at least part of the amyloid fibers.

Alzheimer Disease↗

PubMedDate not supplied

On the relationship between measles virus and Alzheimer neurofibrillary tangles in subacute sclerosing panencephalitis.

We have studied the relationship between measles virus and the accumulation of abnormally phosphorylated tau (PHF-tau) in nine cases of subacute sclerosing panencephalitis (SSPE). By assessing the presence of viral intranuclear inclusions and neurofibrillary tangles (NFT) in each case, we found no correlation between presence and amount of measles virus and the numbers of neurons containing PHF-tau. Immunohistochemical double labeling in a case with long duration of disease and severe histopathologic change revealed no strict colocalization of measles virus antigen and PHF-tau throughout different brain regions. In areas containing both antigens, most neurons carrying measles virus did not have a tangle and vice versa, eventhough some colocalization beyond that expected by chance was observed in specific cortical areas. These results indicate that, although secondary to viral infection, NFT formation in SSPE is not restricted to cells carrying viral antigen. Conversely, measles virus infected cells do not necessarily accumulate PHF-tau. This lack of colocalization at the cellular level, throughout different brain areas and among different cases suggests that the formation of NFT in SSPE is not directly induced by the infectious agent. The formation of NFT in this disease appears to be elicited through a specific type of tissue damage and, thus, to be an epiphenomenon. This pathogenetic detail may be of interest for our understanding of the role of neurofibrillary degeneration in the pathogenesis of other more frequent neurodegenerative diseases with cytoskeletal pathology.

Adolescent↗

PubMedDate not supplied

The role of perivascular and microglial cells in fibrillogenesis of beta-amyloid and PrP protein in Alzheimer's disease and scrapie.

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Alzheimer Disease↗