 |
| Research article summary (published 29 Sep 2003): |
|
Free Full Text! See links below |
Subicular dendritic arborization in Alzheimer's disease correlates with neurofibrillary tangle density.
Full Abstract
Intracellular accumulation of PHFtau in Alzheimer's disease (AD) disrupts the neuronal cytoskeleton and other neuronal machinery and contributes to axonal and dendritic degeneration, and neuronal death. Furthermore, amyloid-beta (Abeta) has been reported to be toxic to neurons and neurites. While loss of presynaptic elements is an established feature of AD, the nature and extent of dendritic degeneration has been infrequently studied. We investigated MAP2-immunoreactive dendrites using a novel method of high-throughput quantification and also measured cortical thickness and the densities of NeuN-immunoreactive neurons, PHFtau neurofibrillary tangles (NFTs), and Abeta plaque burden in the subiculum in AD and elderly controls. Corrected for atrophy, the "dendritic arborization index" was significantly reduced by up to 66% in all three layers of the subiculum. Laminar thickness was reduced by an average 33% and there was a marked reduction in neuron density of approximately 50%. As expected, NFTs and Abeta plaques were significantly increased in AD. Dendritic arborization indices negatively correlated with NFT densities while no significant correlations were found with Abeta plaque densities. The pattern of dendritic loss in the subiculum and the correlations with NFT densities respectively suggest that deafferentation and intrinsic neurofibrillary degeneration both may contribute to dendritic loss in AD.
Learn Faster Today Improve your study skills
Author information
Author/s: Falke, Eric (E); Nissanov, Jonathan (J); Mitchell, Thomas W (TW); Bennett, David A (DA); Trojanowski, John Q (JQ); Arnold, Steven E (SE);
Affiliation: Cellular and Molecular Neuropathology Program, Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Grants: AG09215 (Agency:United States NIA) ; AG10124 (Agency:United States NIA) ; AG15819 (Agency:United States NIA) ; AG17917 (Agency:United States NIA) ; MH57401 (Agency:United States NIMH)
Journal and publication information
Publication Type: Journal Article; Research Support, U.S. Gov't, P.H.S.
Journal: The American journal of pathology (Am J Pathol), published in United States. (Language: eng)
Reference: 2003-Oct; vol 163 (issue 4) : pp 1615-21
Dates: Created 2003/09/25; Completed 2003/10/29; Revised 2007/11/14;
PMID: 14507668, status: MEDLINE (last retrieval date: 11/6/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
External Links for this article (including full text providers, if available):
Click Electronic Full-text Provider Links to see options for finding the electronic full text links to this article. Note there may be a subscription or fee required for access to the full text. See our FAQ for information on finding FREE full text articles.
This article may also be located in paper journal collections available in many libraries. Use the Journal and Publication Information above to find the full article.
MeSH headings (categories)
This article was linked to the MESH Headings shown below.
|
|
Related articles
This article has not been indexed for related articles as yet, however you can still use the live related article search links below.
See a large map of 100+ related articles.