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(American Journal of Pathology. 2003;163:1615-1621.)
© 2003 American Society for Investigative Pathology

Subicular Dendritic Arborization in Alzheimer’s Disease Correlates with Neurofibrillary Tangle Density

Eric Falke^*, Jonathan Nissanov, Thomas W. Mitchell^*, David A. Bennett, John Q. Trojanowski and Steven E. Arnold^*

From the Cellular and Molecular Neuropathology Program,^* Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania; the Computer Vision Laboratory for Vertebrate Brain Mapping, Department of Neurobiology and Anatomy, Drexel University, Philadelphia, Pennsylvania; the Rush Alzheimer’s Disease Center and Department of Neurological Sciences, Rush-Presbyterian St. Luke’s Medical Center, Chicago, Illinois; and the Center for Neurodegenerative Disease Research and Institute on Aging, University of Pennsylvania, Philadelphia, Pennsylvania

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-ß (Aß) 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 Aß 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 Aß plaques were significantly increased in AD. Dendritic arborization indices negatively correlated with NFT densities while no significant correlations were found with Aß 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.

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