Reduction of Acetylated a-Tubulin Immunoreactivity in Neurofibrillary Tangle-bearing Neurons in Alzheimer's Disease (original) (raw)
Journal Article
,
Laboratory of Pathology,
Université Libre de Bruxelles
, Faculté de Medicine, Route de Lennik 808, Bldg C-10, B-1070 Brussels, Belgium
Electron Microscopy,
Université Libre de Bruxelles
, Faculté de Medicine, Route de Lennik 808, Bldg C-10, B-1070 Brussels, Belgium
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Laboratory of Pathology,
Université Libre de Bruxelles
, Faculté de Medicine, Route de Lennik 808, Bldg C-10, B-1070 Brussels, Belgium
Electron Microscopy,
Université Libre de Bruxelles
, Faculté de Medicine, Route de Lennik 808, Bldg C-10, B-1070 Brussels, Belgium
Correspondence to: Dr J.P. Brion, Laboratory of Pathology and Electron Microscopy, Université Libre de Bruxelles, Route de Lennik 808, Bldg C-10, B-1070 Brussels, Belgium.
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This study was supported by grants from the Belgian FRSM (n°3.4507.95) and from Alzheimer Belgique.
Published:
01 September 1996
Cite
Bart Hempen, Jean-Pierre Brion, Reduction of Acetylated a-Tubulin Immunoreactivity in Neurofibrillary Tangle-bearing Neurons in Alzheimer's Disease, Journal of Neuropathology & Experimental Neurology, Volume 55, Issue 9, September 1996, Pages 964–972, https://doi.org/10.1097/00005072-199609000-00003
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Abstract
A disturbance of the microtubule network in neurons containing neurofibrillary tangles (NFT), one of the characteristic neuropathological lesions in Alzheimer's disease, has been advocated as a central physiopathological mechanism leading to neuronal dysfunction in NFT-containing neurons. The accumulation of “paired helical filament-tau,” the main proteineous component of NFT, in affected neurons has been proposed to induce a decrease of microtubule stability in these cells. To further explore the hypothesis of a decrease in microtubule stability in Alzheimer's disease, we have investigated in this study the relative content in stable microtubules in neurons with different amount of NFT. We used a double immuno-cytochemical labeling technique with antibodies to tau (as a marker of NFT) and to acetylated α-tubulin (as a marker of stable microtubules) and rated on a semi-quantitative scale the tau and acetylated a-tubulin-immunoreactivities in the same neurons. We observed a strong reduction in acetylated α-tubulin immunoreactivity in most NFT-bearing neurons; a statistical relationship between tau and acetylated α-tubulin immunoreactivity was demonstrated, assuming an inverse relationship between the presence of tau-immunoreactive NFT and tubulin-immunoreactivity in neurons. This reduction was already seen in the neuronal population with a relatively lower tau-immunoreactivity, suggesting that reduction in acetylated α-tubulin immunoreactivity, and reduction in microtubule stability, could be an early event in these cells.
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Author notes
This study was supported by grants from the Belgian FRSM (n°3.4507.95) and from Alzheimer Belgique.
© 1996 by the American Association of Neuropathologists, Inc.
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