Decreased Oligodendrocyte Nuclear Diameter in Alzheimer's Disease and Lewy Body Dementia

To better understand the pathogenesis of dementia, it is important to understand histopathologic changes in neurodegenerative diseases because they might highlight key aspects of the degenerative process. In this study, the nuclear diameter of neurons and oligodendrocytes in selected temporal lobe a...

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Published in:Brain pathology (Zurich, Switzerland) Vol. 22; no. 6; pp. 803 - 810
Main Authors: Gagyi, Eva, Kormos, Bernadett, Castellanos, Karla J., Valyi-Nagy, Klara, Korneff, Dennis, LoPresti, Patrizia, Woltjer, Randy, Valyi-Nagy, Tibor
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 01-11-2012
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Summary:To better understand the pathogenesis of dementia, it is important to understand histopathologic changes in neurodegenerative diseases because they might highlight key aspects of the degenerative process. In this study, the nuclear diameter of neurons and oligodendrocytes in selected temporal lobe areas were determined in autopsy tissue sections from patients with Alzheimer's disease (AD), Lewy body dementia (LBD) and controls. Our morphometric studies targeted neurons in the CA4 region of the pyramidal cell layer of the hippocampus, neurons in the granular layer of the dentate gyrus and oligodendrocytes in parahippocampal white matter. Mean neuronal nuclear diameters were not different among the studied groups. However, our studies revealed a statistically significant reduction of mean oligodendrocyte nuclear diameter in AD and LBD relative to controls. The reduction of the mean nucleus diameter of oligodendrocytes in LBD was independent of the presence of associated AD pathology in LBD. These findings for the first time identify decreased oligodendrocyte nucleus diameter as a morphologic feature of AD and LBD and may lead to a better understanding of the role of oligodendrocytes in AD and LBD pathogenesis.
Bibliography:istex:91625AE03F7D437E2216E58832056290CF11A984
ArticleID:BPA595
ark:/67375/WNG-TWP7570K-1
These authors contributed equally.
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ISSN:1015-6305
1750-3639
DOI:10.1111/j.1750-3639.2012.00595.x