title: Immunocytochemical analysis of tumor necrosis factor and its receptors in Parkinson's disease.
abstract: Activated glial cells observed in the substantia nigra in Parkinson's disease may participate in the mechanism of nerve cell death by providing toxic substances such as cytokines. Among these compounds, tumor necrosis factor-alpha (TNF) is of interest because it can provoke cell death. We detected TNF-immunoreactive glial cells in the substantia nigra of parkinsonian patients but not in those of control subjects. Immunoreactivity for TNF receptors was found in cell bodies and processes of most dopaminergic neurons of control and parkinsonian subjects, suggesting that nigral dopaminergic neurons might be sensitive to TNF produced in Parkinson's disease. These results suggest that TNF may participate in the degenerative processes occurring in Parkinson's disease, at least after a primary insult inducing a reactive gliosis.
authors.affiliation: INSERM U289, Hôpital de la Salpêtrière, Paris, France.
authors.forename: G
authors.initials: G
authors.lastname: Boka
authors.forename: P
authors.initials: P
authors.lastname: Anglade
authors.forename: D
authors.initials: D
authors.lastname: Wallach
authors.forename: F
authors.initials: F
authors.lastname: Javoy-Agid
authors.forename: Y
authors.initials: Y
authors.lastname: Agid
authors.forename: E C
authors.initials: EC
authors.lastname: Hirsch
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D004298:Dopamine / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D009457:Neuroglia / Q000276:immunology / Q000378:metabolism; D010300:Parkinson Disease / Q000378:metabolism* / Q000473:pathology; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis* / Q000276:immunology; D013378:Substantia Nigra / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000276:immunology
chemical_list: D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D004298:Dopamine