Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 3 July 1987:
Vol. 237. no. 4810, pp. 77 - 80
DOI: 10.1126/science.3299701

Articles

Science, Vol 237, Issue 4810, 77-80
Copyright © 1987 by American Association for the Advancement of Science


articles

Localization of amyloid beta protein messenger RNA in brains from patients with Alzheimer's disease

S Bahmanyar, GA Higgins, D Goldgaber, DA Lewis, JH Morrison, MC Wilson, SK Shankar, and DC Gajdusek

The distribution of cells containing messenger RNA that encodes amyloid beta protein was determined in hippocampi and in various cortical regions from cynomolgus monkeys, normal humans, and patients with Alzheimer's disease by in situ hybridization. Both 35S-labeled RNA antisense and sense probes to amyloid beta protein messenger RNA were used to ensure specific hybridization. Messenger RNA for amyloid beta protein was expressed in a subset of neurons in the prefrontal cortex from monkeys, normal humans, and patients with Alzheimer's disease. This messenger RNA was also present in the neurons of all the hippocampal fields from monkeys, normal humans and, although to a lesser extent in cornu ammonis 1, patients with Alzheimer's disease. The distribution of amyloid beta protein messenger RNA was similar to that of the neurofibrillary tangles of Alzheimer's disease in some regions, but the messenger RNA was also expressed in other neurons that are not usually involved in the pathology of Alzheimer's disease.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Amyloid Precursor Protein and Mitochondrial Dysfunction in Alzheimer's Disease.
H. K. Anandatheerthavarada and L. Devi (2007)
Neuroscientist 13, 626-638
   Abstract »    PDF »
Increased Risk of Type 2 Diabetes in Alzheimer Disease.
J. Janson, T. Laedtke, J. E. Parisi, P. O'Brien, R. C. Petersen, and P. C. Butler (2004)
Diabetes 53, 474-481
   Abstract »    Full Text »
Fine mapping of the {alpha}-T catenin gene to a quantitative trait locus on chromosome 10 in late-onset Alzheimer's disease pedigrees.
N. Ertekin-Taner, J. Ronald, H. Asahara, L. Younkin, M. Hella, S. Jain, E. Gnida, S. Younkin, D. Fadale, Y. Ohyagi, et al. (2003)
Hum. Mol. Genet. 12, 3133-3143
   Abstract »    Full Text »    PDF »
Transcriptional regulation of Alzheimer's disease genes: implications for susceptibility.
J. Theuns and C. Van Broeckhoven (2000)
Hum. Mol. Genet. 9, 2383-2394
   Abstract »    Full Text »    PDF »
Relative Increase in Alzheimer's Disease of Soluble Forms of Cerebral Abeta Amyloid Protein Precursor Containing the Kunitz Protease Inhibitory Domain.
R. D. Moir, T. Lynch, A. I. Bush, S. Whyte, A. Henry, S. Portbury, G. Multhaup, D. H. Small, R. E. Tanzi, K. Beyreuther, et al. (1998)
J. Biol. Chem. 273, 5013-5019
   Abstract »    Full Text »    PDF »
The Molecular Genetic Revolution: Its Impact on Clinical Neurology.
C. S. Payne and A. D. Roses (1988)
Arch Neurol 45, 1366-1376
   Abstract »    PDF »
Amyloid protein precursor messenger RNAs: differential expression in Alzheimer's disease.
M. Palmert, T. Golde, M. Cohen, D. Kovacs, R. Tanzi, J. Gusella, M. Usiak, L. Younkin, and S. Younkin (1988)
Science 241, 1080-1084
   Abstract »    PDF »



To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)