| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Journal of Pathology, Vol 136, 1069-1075, Copyright © 1990 by American Society for Investigative Pathology
REGULAR ARTICLES |
ML Schmidt, VM Lee and JQ Trojanowski
Department of Pathology and Laboratory Medicine (Neuropathology), University of Pennsylvania School of Medicine, Philadelphia 19104-4283.
Neurofibrillary tangles (NFTs) derive, in part, from normal neuronal cytoskeletal proteins, ie, large portions of tau (tau) but only restricted segments of the peripheral domains of the high- and middle- molecular weight neurofilament subunits. To learn more about the events leading to the incorporation of tau and neurofilament epitopes into NFTs, the relative abundance of tau and NF determinants in these lesions was quantitatively analyzed in hippocampi from Alzheimer disease (AD) patients and age-matched controls using monoclonal antibodies specific for tau or for NF proteins. Immunostained NFTs appeared qualitatively the same in both AD and controls, ie, every epitope found in AD NFTs occurred also in the NFTs of the control patients. However, in hippocampi with only a few tangles, tau epitopes, but no NF epitopes, were detected in NFTs. In contrast, both tau and NF epitopes were present in those tangles that were found in hippocampi with abundant NFTs. Nevertheless, the number of tau-positive NFTs generally exceeded the number of NF-positive NFTs. These findings indicate that tau epitopes are more abundant than NF epitopes in NFTs and that the formation of NFTs may be linked to a derangement in the normal metabolism of tau that is more extensive than alterations in NF protein metabolism.
This article has been cited by other articles:
 |
|
 |
|
  L. Lyck, I. Dalmau, J. Chemnitz, B. Finsen, and H. D. Schroder Immunohistochemical Markers for Quantitative Studies of Neurons and Glia in Human Neocortex J. Histochem. Cytochem., March 1, 2008; 56(3): 201 - 221. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. J. Cairns, M. Grossman, S. E. Arnold, D. J. Burn, E. Jaros, R. H. Perry, C. Duyckaerts, B. Stankoff, B. Pillon, K. Skullerud, et al. Clinical and neuropathologic variation in neuronal intermediate filament inclusion disease Neurology, October 26, 2004; 63(8): 1376 - 1384. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. E. Arnold, L.-Y. Han, P. J. Moberg, B. I. Turetsky, R. E. Gur, J. Q. Trojanowski, and C.-G. Hahn Dysregulation of Olfactory Receptor Neuron Lineage in Schizophrenia Arch Gen Psychiatry, September 1, 2001; 58(9): 829 - 835. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ishihara, M. Higuchi, B. Zhang, Y. Yoshiyama, M. Hong, J. Q. Trojanowski, and V. M.-Y. Lee Attenuated Neurodegenerative Disease Phenotype in Tau Transgenic Mouse Lacking Neurofilaments J. Neurosci., August 15, 2001; 21(16): 6026 - 6035. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. M.-Y. Lee and J. Q. Trojanowski Transgenic mouse models of tauopathies: Prospects for animal models of Pick's disease Neurology, June 12, 2001; 56(90004): S26 - 30. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H. Morrison and P. R. Hof Life and Death of Neurons in the Aging Brain Science, October 17, 1997; 278(5337): 412 - 419. [Abstract] [Full Text]
|
|
|
|
|
|
V. Lee, B. Balin, L Otvos Jr, and J. Trojanowski A68: a major subunit of paired helical filaments and derivatized forms of normal Tau Science, February 8, 1991; 251(4994): 675 - 678. [Abstract] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
