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.


Science 30 October 1987:
Vol. 238. no. 4827, pp. 666 - 669
DOI: 10.1126/science.2890207

Articles

Science, Vol 238, Issue 4827, 666-669
Copyright © 1987 by American Association for the Advancement of Science


articles

The amyloid beta protein gene is not duplicated in brains from patients with Alzheimer's disease

RE Tanzi, ED Bird, SA Latt, and RL Neve

Division of Genetics and Mental Retardation Center, Children's Hospital, Boston, MA.

Complementary DNAs (cDNAs) encoding portions of the amyloid beta protein were used to investigate possible amyloid gene duplication in sporadic Alzheimer's disease. A strategy employing two Eco RI restriction fragment length polymorphisms (RFLPs) detected by the amyloid cDNAs was used. RFLPs allow the detection of a 2:1 gene dosage in the DNA of any individual who is heterozygous for a particular RFLP. The amyloid gene regions homologous to the cDNAs used were not duplicated in the DNA from brains of individuals with sporadic Alzheimer's disease. Similar results were also obtained with a strategy employing a test for 3:2 gene dosage.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
The Effect of A{beta} Conformation on the Metal Affinity and Aggregation Mechanism Studied by Circular Dichroism Spectroscopy..
Y.R. Chen, H.B. Huang, C.L. Chyan, M.S. Shiao, T.H. Lin, and Y.C. Chen (2006)
J. Biochem. 139, 733-740
   Abstract »    Full Text »    PDF »
APP-BP1, a Novel Protein That Binds to the Carboxyl-terminal Region of the Amyloid Precursor Protein.
N. Chow, J. R. Korenberg, X.-N. Chen, and R. L. Neve (1996)
J. Biol. Chem. 271, 11339-11346
   Abstract »    Full Text »    PDF »
Association of Decreased Paternal Age and Late-Onset Alzheimer's Disease: An Example of Genetic Imprinting?.
L. A. Farrer, L. A. Cupples, L. Connor, P. A. Wolf, and J. H. Growdon (1991)
Arch Neurol 48, 599-604
   Abstract »    PDF »
Natural Killer Cell Activity in Patients With Dementia of the Alzheimer Type.
S. Araga, H. Kagimoto, K. Funamoto, A. Adachi, K. Inoue, and K. Takahashi (1990)
Arch Neurol 47, 380-381
   Abstract »    PDF »
Amyloid beta protein enhances the survival of hippocampal neurons in vitro.
J. Whitson, D. Selkoe, and C. Cotman (1989)
Science 243, 1488-1490
   Abstract »    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 »
Biologic Markers, Genetics, and Alzheimer's Disease.
G. W. Small and D. A. Greenberg (1988)
Arch Gen Psychiatry 45, 945-947
   Abstract »    PDF »
Role of Alzheimer's protein is tangled.
J. Mark (1987)
Science 238, 1352-1353
   PDF »



To Advertise     Find Products


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