ON THE RELATIONSHIP BETWEEN MEASLES-VIRUS AND ALZHEIMER NEUROFIBRILLARY TANGLES IN SUBACUTE SCLEROSING PANENCEPHALITIS

Citation
C. Bancher et al., ON THE RELATIONSHIP BETWEEN MEASLES-VIRUS AND ALZHEIMER NEUROFIBRILLARY TANGLES IN SUBACUTE SCLEROSING PANENCEPHALITIS, Neurobiology of aging, 17(4), 1996, pp. 527-533
Citations number
43
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
01974580
Volume
17
Issue
4
Year of publication
1996
Pages
527 - 533
Database
ISI
SICI code
0197-4580(1996)17:4<527:OTRBMA>2.0.ZU;2-E
Abstract
We have studied the relationship between measles virus and the accumul ation of abnormally phosphorylated tau (PHF-tau) in nine cases of suba cute sclerosing panencephalitis (SSPE). By assessing the presence of v iral 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. Immunohistochemic al double labeling in a case with long duration of disease and severe histopathologic change revealed no strict colocalization of measles vi rus antigen and PHF-tau throughout different brain regions. In areas c ontaining both antigens, most neurons carrying measles virus did not h ave a tangle and vice versa, even though some colocalization beyond th at expected by chance was observed in specific cortical areas. These r esults indicate that, although secondary to viral infection, NFT forma tion in SPE is not restricted to cells carrying viral antigen. Convers ely, measles virus infected cells do not necessarily accumulate PHF-ta u. This lack of colocalization at the cellular level, throughout diffe rent brain areas and among different cases suggests that the formation of NFT in SSPE is not directly induced by the infectious agent. The f ormation of NFT in this disease appears to be elicited through a speci fic type of tissue damage and, thus, to be an epiphenomenon. This path ogenetic detail may be of interest for our understanding of the role o f neurofibrillary degeneration in the pathogenesis of other more frequ ent neurodegenerative diseases with cytoskeletal pathology.