Summary
The prevalance of pale bodies and Lewy bodies was studied in the substantia nigra of 12 patients with typical Parkinson's disease (PD), in 5 patients with diffuse Lewy body disease (DLBD), and in a group of neurologically normal controls. Anti-ubiquitin antibodies labelled pale bodies and Lewy bodies in typical PD and DLBD, and there was a strong positive correlation between numbers of ubiquitin-immunoreactive pale bodies and Lewy bodies. BF10, a monoclonal antibody against a phosphate-dependent epitope of neurofilament 155-kDa polypeptide subunit, immunolabelled 57% of Lewy bodies and 15% of pale bodies in typical PD. Some pale bodies and Lewy bodies were seen in the substantia nigra of 2 of 5 neurologically normal, aged controls, probably representing “incidental PD”. We conclude that there is a close relationship between pale bodies and typical Lewy bodies in the substantia nigra in clinical varicties of PD, and that these inclusions share antigenic determinants. If pale bodies and Lewy bodies reflect separate aspects of the cellular pathology in PD, their formation probably occurs in parallel. Alternatively, these observations may suggest that pale bodies represent a stage in the formation of Lewy bodies.
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Anderton BH, Breiburg D, Downes MJ, Green PJ, Tomlinson BE, Ulrich E, Wood JN, Kahn J (1982) Monoclonal antibodies show that neurofibrillary tangles and neurofilaments share antigenic determinants. Nature 298:84–86
Bancher C, Lasmann H, Budka H, Jellinger K, Grundke-Iqbal I, Iqbal K, Wiche G, Seitelberger F, Wisniewski HM (1989) An antigenic profile of Lewy bodies: immunocytochemical indication for protein phosphorylation and ubiquitination. J Neuropathol Exp Neurol 48:81–93
Cole GM, Timiras PS (1987) Ubiquitin-protein conjugates in Alzheimer's lesions. Neurosci Lett 79:207–212
Dickson DW, Crystal H, Mattiace LA, Kress Y, Schwagerl A, Ksiezak-Reding H, Davies P, Yen S-HC (1989) Diffuse Lewy body disease: light and electron microscopic immunocytochemistry of senile plaques. Acta Neuropathol 78:572–584
Forno LS, Sternberger LA, Sternberger NH, Strefling AM, Swanson K, Eng LF (1986) Reaction of Lewy bodies to phosphorylated and non-phosphorylated neurofilaments. Neurosci Lett 64:253–258
Galloway PG, Grundke-Iqbal I, Iqbal K, Perry G (1986) Lewy bodies contain epitopes both shared and distinct from Alzheimer neurofibrillary tangles. J Neuropathol Exp Neurol 47:654–663
Galloway PG, Bergeron C, Perry G (1989) The presence of tau distinguishes Lewy bodies of diffuse Lewy body disease from those of idiopathic Parkinson's disease. Neurosci Lett 110:6–10
Gibb WRG, Lees AJ (1988) The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson's disease. J Neurol Neurosurg Psychiatry 51:745–752
Gibb WRG, Lees AJ (1989) The significance of the Lewy body in the diagnosis of idiopathic Parkinson's disease. Neuropathol Appl Neurobiol 15:27–44
Gibb WRG, Luthert PJ, marsden CD (1989) corticobasal degeneration. Brain 112:1171–1192
Gibb WRG, Scott T, Lees AJ (1990) The neuronal inclusions of Parkinson's disease. Mov Disord (in press)
Goldman JE (1987) Cytoskeletal abnormalities in Parkinson's disease. In: Perry G (ed) Alterations of the neuronal cytoskeleton in Alzheimer's disease. Plenum Press, New York, pp 191–197
Goldman JE, Yen S-H (1986) Cytoskeletal protein abnormalities in neurodegenerative diseases. Ann Neurol 19:209–223
Goldman JE, Yen S-H, Chiu FC, Peress NS (1983) Lewy bodies of Parkinson's disease contain neurofilament antigens. Science 221:1082–1084
Greenfield JG, Bosanquet FD (1953) The brain stem lesions in parkinsonism. J Neurol Neurosurg Psychiatry 16:213–226
Hassler R (1938) Zur Pathologie der Paralysis agitans und des postenzephalitischen Parkinsonismus. J Psychol Neurol 51:745–746
Haugh MC, Probst, A, Ulrich J, Kahn J, Anderton BH (1986) Alzheimer neurofibrillary tangles contain phosphorylated and hidden neurofilament proteins. J Neurol Neurosurg Psychiatry 49:1213–1220
Kahn J, Anderton BH, Gibb WRG, Lees AJ, Wells FR, Marsden CD (1985) Neuronal filaments in Alzheimer's, Pick's and Parkinson's diseases. N Engl J Med 313:520–521
Kuzuhara S, Mori H, Isumiyama M, Yoshimura M, Ihara Y (1988) Lewy bodies are ubiquitinated. A light and microscopic immunocytochemical study. Acta Neuropathol (Berl) 75:345–353
Leigh PN, Anderton BH, Dodson A, Gallo J-M, Swash M, Power DM (1988) Ubiquitin deposits in motor neurone disease. Neurosci Lett 93:197–203
Leigh PN, Probst A, Dale GE, Power DP, Brion J-P, Dodson A, Anderton BH (1989) New aspects of the pathology of neurodegenerative disorders as revealed by ubiquitin antibodies. Acta Neuropathol 79:61–72
Lennox G, Lowe J, Morrell K, Landon M, Mayer RJ (1988) Anti-ubiquitin immunocytochemistry is more sensitive than conventional techniques in the detection of diffuse Lewy body disease. J Neurol Neurosurg Psychiatry 51:67–71
Love S, Saitoh T, Saitoh T, Quijada S, Cole GM, Terry RD (1988) Alz-50, ubiquitin, and tau reactivity of neurofibrillary tangles, Pick bodies and Lewy bodies, J Neuropathol Exp Neurol 47:393–405
Lowe J, Lennox G, Jefferson D, Morrell K, McQuire D, Gray T, Landon M, Doherty FJ, Mayer RJ (1988) A filamentous inclusion body within anterior horn neurones in motor neurone disease defined by immunocytochemical localisation of ubiquitin. Neurosci Lett 94:203–210
Lowe J, Blanchard A, Morrell K, Lennox G, Reynolds L, Billet M, Landon M, Mayer RJ (1988) Ubiquitin is a common factor in intermediate filament inclusion bodies of diverse type in man, including those of Parkinson's disease, Pick's disease, and Alzheimer's disease, as well as Rosenthal fibres in cerebellar astrocytomas, cytoplasmic bodies in muscle, and Mallory bodies in alcoholic liver disease. J Pathol 155:9–15
Manetto V, Abdul-Karim FW, Perry G, Tabaton M, Autilio-Gambetti L, Gambetti P (1989) Selective presence of ubiquitin in intracellular inclusions. Am J Pathol 134:505–513
Miller CCJ, Brion J-P, Calvert R, Chin TK, Eagles PAM, Downes MJ, Flament-Durand J, Haugh M, Kahn J, Probst A, Ulrich J, Anderton BH (1986) Alzheimer's paired helical filaments share epitopes with neurofilament side arms. EMBO J 5:269–276
Mori H, Kondon J, Ihara Y (1986) Ubiquitin is a component of paired helical filaments in Alzheimer's disease. Science 235:1641–1646
Nobrega FT, Glattre E, Kurland LT, et al (1969) Comments on the epidemiology of parkinsonism, including prevalence and incidence statistics from Rochester, Minnesota, 1953–6. In: Barbeau A, Brunette JR (eds) Progress in neurogenetics. Excerpta Medica, Amsterdam, pp 472–485
Pappolla MA, Shank DL, Alzofon J, Dudley AW (1988) Colloid (hyaline) inclusion bodies in the central nervous system: their presence in the substantia nigra is dignostic of Parkinson's disease. Hum Pathol 19:27–31
Paulus W, Selim M (1990) Corticonigral degeneration with neuronal achromasia and basal neurofibrillary tangles. Acta Neuropathol 81:89–94
Perry G, Friedman R, Shaw G, Chan V (1987) Ubiquitin is detected in neurofibrillary tangles and senile plaque neurites in Alzheimer's disease brains. Procl Natl Acad Sci USA 84:3033–3036
Probst A, Dufresne JJ (1977) Dégénérescence neurofibrillaire sous-corticale. Présence de tubules et de filaments droits Forme atypique de la paralyse supranucléare progressive. Rev Neurol (Paris) 33:417–428
Rechsteiner M (1987) Ubiquitin-mediated pathways for intracellular proteolysis. Annu Rev Cell Biol 3:1–30
Tellez-Nagel I, Wisziewski HM (1973) Ultrastructure of neurofibrillary tangles in Steele-Richardson-Olszewski syndrome. Arch Neurol 29:324–327
Ulrich J, Haugh M, Anderton BH, Probst A, Lautenschlager C, His B (1987) Alzheimer's dementia and Pick's disease are associated with identical phosphorlyted neurofilament epitopes. Acta Neuropathol (Berl) 73:240–246
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Supported by the Medical Research Council, the Wellcome Trust, and the Parkinson's Disease Society of Great Britain
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Dale, G.E., Probst, A., Luthert, P. et al. Relationships between Lewy bodies and pale bodies in Parkinson's disease. Acta Neuropathol 83, 525–529 (1992). https://doi.org/10.1007/BF00310030
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DOI: https://doi.org/10.1007/BF00310030