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Immunohistochemical characterization and quantification of Marinesco bodies in Alzheimer's and Parkinson's diseases
Author(s) -
Vollans A. K.,
Shukla C.,
Bridges L. R.
Publication year - 2002
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.2002.39286_48.x
Subject(s) - neurodegeneration , substantia nigra , pathology , alzheimer's disease , parkinson's disease , biology , midbrain , disease , degenerative disease , amyloid (mycology) , immunohistochemistry , medicine , neuroscience , central nervous system
Marinesco bodies (MBs) were described 100 years ago but, unlike the intranuclear inclusions in the triplet repeat diseases, have received little attention in the literature. Our aim was to see whether they are disease associated or purely age related. Materials and methods: We examined 15 cases each of Alzheimer's disease, Parkinson's disease and age‐matched control brains. Paraffin sections of midbrain were cut in thicknesses of 5 µm, and immunostained with α‐synuclein and ubiquitin (Novocastra) and tau, β‐amyloid and PrP (Dako). Staining was enhanced with Envision (Dako). A blue‐grey chromagen (Vector SG, Vector) was chosen to provide contrast with the brown pigment of the substantia nigra neurons. Results: MBs were immunopositive for ubiquitin but not for α‐synuclein, tau, β‐amyloid and PrP. Within affected neurons, MB were fewer in Parkinson's disease than in Alzheimer's disease and ‘normals’ (medians 1.48, 1.98 and 2.00 respectively; P < 0.01). Within normals, the size of MB‐affected neurons was significantly less than that of MB‐unaffected neurons (median areas 605 and 969 µm 2 respectively; P < 0.01). MB relative to cell size were smaller in Parkinson's disease than Alzheimer's disease and controls (medians 0.86, 1.07 and 1.12% respectively; P < 0.01). Conclusions: Differences exist between number and size of Marinesco bodies and affected neurons in neurodegeneration and normal ageing, but there is no clear evidence of a disease association.