help button home button Am J Pathol International Conference on Pathology of Chest Diseases
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 Murphy, G. M.
Right arrow Articles by Cordell, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Murphy, G. M., Jr
Right arrow Articles by Cordell, B.

American Journal of Pathology, Vol 144, 1082-1088, Copyright © 1994 by American Society for Investigative Pathology

REGULAR ARTICLES

Development of a monoclonal antibody specific for the COOH-terminal of beta-amyloid 1-42 and its immunohistochemical reactivity in Alzheimer's disease and related disorders

GM Murphy Jr, LS Forno, L Higgins, JM Scardina, LF Eng and B Cordell
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, California.

The beta-amyloid peptide (beta AP) has been characterized by protein sequencing techniques as a 39-43 amino acid protein with heterogeneous COOH-termini. Controversy exists regarding the predominant form of beta AP in neuritic plaques (NP) and cerebral vasculature of Alzheimer's disease (AD) brain. A monoclonal antibody was developed that selectively recognizes the free COOH-terminal of beta AP 1-42 but not beta AP species with shorter or longer COOH-termini. Brain sections from AD and related disorders were examined using this antibody. In AD samples, the antibody stained diffuse amyloid and NP cores, many intraneuronal and extraneuronal neurofibrillary tangles (NFT), but not cerebrovascular amyloid. Pick and Lewy bodies lacked immunoreactivity. These findings suggest that beta AP 1-42 is present in early and mature amyloid deposits and NFT, but that species of beta AP other than 1-42 comprise human vascular deposits.


This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
X.-H. Chen, R. Siman, A. Iwata, D. F. Meaney, J. Q. Trojanowski, and D. H. Smith
Long-Term Accumulation of Amyloid-{beta}, {beta}-Secretase, Presenilin-1, and Caspase-3 in Damaged Axons Following Brain Trauma
Am. J. Pathol., August 1, 2004; 165(2): 357 - 371.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. S. Atwood, R. D. Moir, X. Huang, R. C. Scarpa, N. M. E. Bacarra, D. M. Romano, M. A. Hartshorn, R. E. Tanzi, and A. I. Bush
Dramatic Aggregation of Alzheimer Abeta by Cu(II) Is Induced by Conditions Representing Physiological Acidosis
J. Biol. Chem., May 22, 1998; 273(21): 12817 - 12826.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. A. Golabek, C. Soto, T. Vogel, and T. Wisniewski
The Interaction between Apolipoprotein E and Alzheimer's Amyloid beta-Peptide Is Dependent on beta-Peptide Conformation
J. Biol. Chem., May 3, 1996; 271(18): 10602 - 10606.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
L. Gregori, C. Fuchs, M. E. Figueiredo-Pereira, W. E. Van Nostrand, and D. Goldgaber
Amyloid beta-Protein Inhibits Ubiquitin-dependent Protein Degradation in Vitro
J. Biol. Chem., August 25, 1995; 270(34): 19702 - 19708.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1994 by the American Society for Investigative Pathology.