help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Iwatsubo, T.
Right arrow Articles by Trojanowski, J. Q.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Iwatsubo, T.
Right arrow Articles by Trojanowski, J. Q.

American Journal of Pathology, Vol 149, 1823-1830, Copyright © 1996 by American Society for Investigative Pathology

REGULAR ARTICLES

Full-length amyloid-beta (1-42(43)) and amino-terminally modified and truncated amyloid-beta 42(43) deposit in diffuse plaques

T Iwatsubo, TC Saido, DM Mann, VM Lee and JQ Trojanowski
Department of Neuropathology and Neuroscience, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.

The amino- and carboxyl-terminal properties of the amyloid-beta (A beta) peptides deposited in diffuse plaques, one of the earliest forms of A beta deposition, were examined in the brains of patients with Down's syndrome and Alzheimer's disease and in aged individuals without dementia by immunocytochemistry. This was done using a panel of antibodies that specifically discriminate the terminal structures and modifications at the amino and carboxyl termini of A beta. Diffuse plaques found in the cerebral and cerebellar cortex, neostriatum, and hypothalamus of Down's syndrome, Alzheimer's disease, and nondemented brains were strongly immunoreactive for A beta N1(L-Asp), A beta N1(L- isoAsp), A beta N1(D-Asp), and A beta N3(pyroGlu) and weakly positive for A beta N11(pyroGlu) and A beta N17(Leu). Diffuse plaques also were positive for A beta 42(43) but negative for A beta 40, using carboxyl- terminal-specific anti-A beta antibodies. These results suggest that the amino termini of the A beta species that initially deposit in diffuse plaques begin with A beta N1(Asp) with or without structural modifications (isomerization and racemization), as well as with A beta N3(pyroGlu), and terminate preferentially at A beta 42(43) rather than A beta 40.


This article has been cited by other articles:


Home page
 Sci Aging Knowl EnvironHome page
D. R. Thal, E. Capetillo-Zarate, K. Del Tredici, and H. Braak
The Development of Amyloid beta Protein Deposits in the Aged Brain
Sci. Aging Knowl. Environ., March 8, 2006; 2006(6): re1 - re1.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Y. Tomidokoro, T. Lashley, A. Rostagno, T. A. Neubert, M. Bojsen-Moller, H. Braendgaard, G. Plant, J. Holton, B. Frangione, T. Revesz, et al.
Familial Danish Dementia: CO-EXISTENCE OF DANISH AND ALZHEIMER AMYLOID SUBUNITS (ADan AND A{beta}) IN THE ABSENCE OF COMPACT PLAQUES
J. Biol. Chem., November 4, 2005; 280(44): 36883 - 36894.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
M. M. Racke, L. I. Boone, D. L. Hepburn, M. Parsadainian, M. T. Bryan, D. K. Ness, K. S. Piroozi, W. H. Jordan, D. D. Brown, W. P. Hoffman, et al.
Exacerbation of Cerebral Amyloid Angiopathy-Associated Microhemorrhage in Amyloid Precursor Protein Transgenic Mice by Immunotherapy Is Dependent on Antibody Recognition of Deposited Forms of Amyloid {beta}
J. Neurosci., January 19, 2005; 25(3): 629 - 636.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
V. Koppaka, C. Paul, I. V. J. Murray, and P. H. Axelsen
Early Synergy between A{beta}42 and Oxidatively Damaged Membranes in Promoting Amyloid Fibril Formation by A{beta}40
J. Biol. Chem., September 19, 2003; 278(38): 36277 - 36284.
[Abstract] [Full Text] [PDF]

Home page
 BrainHome page
A. B. Singleton, R. Hall, C. G. Ballard, R. H. Perry, J. H. Xuereb, D. C. Rubinsztein, C. Tysoe, P. Matthews, B. Cordell, S. Kumar-Singh, et al.
Pathology of early-onset Alzheimer's disease cases bearing the Thr113-114ins presenilin-1 mutation
Brain, December 1, 2000; 123(12): 2467 - 2474.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
A. Takeuchi, M. C. Irizarry, K. Duff, T. C. Saido, K. Hsiao Ashe, M. Hasegawa, D. M. A. Mann, B. T. Hyman, and T. Iwatsubo
Age-Related Amyloid {beta} Deposition in Transgenic Mice Overexpressing Both Alzheimer Mutant Presenilin 1 and Amyloid {beta} Precursor Protein Swedish Mutant Is Not Associated with Global Neuronal Loss
Am. J. Pathol., July 1, 2000; 157(1): 331 - 339.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
R. P. Mason, R. F. Jacob, M. F. Walter, P. E. Mason, N. A. Avdulov, S. V. Chochina, U. Igbavboa, and W. G. Wood
Distribution and Fluidizing Action of Soluble and Aggregated Amyloid beta -Peptide in Rat Synaptic Plasma Membranes
J. Biol. Chem., June 25, 1999; 274(26): 18801 - 18807.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
D. W. Dickson
Microglia in Alzheimer's Disease and Transgenic Models : How Close the Fit?
Am. J. Pathol., June 1, 1999; 154(6): 1627 - 1631.
[Full Text] [PDF]

Home page
 J. Neurosci.Home page
T. P. Wong, T. Debeir, K. Duff, and A. C. Cuello
Reorganization of Cholinergic Terminals in the Cerebral Cortex and Hippocampus in Transgenic Mice Carrying Mutated Presenilin-1 and Amyloid Precursor Protein Transgenes
J. Neurosci., April 1, 1999; 19(7): 2706 - 2716.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by the American Society for Investigative Pathology.