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Molecular Biology of Alzheimer's Disease

Molecular Biology of Alzheimer's Disease SUMMARY AND PERSPECTIVES The amyloid first seen by Alois Alzheimer in the brain of a deceased demented patient (1) turned out to be an extraordinary challenge for biochem­ ists and molecular biologists alike. The extreme insolubility of this polypeptide first challenged the protein chemists attempting to sequence it (2, 3). Then Ithe questions arose: Was the amyloid the product of a slow virus (4) or was it the product of a human gene? If the latter, did the structure of its 0066-4154/0701-0287$02.00 MULLER-HILL & BEYREUTHER gene in an Alzheimer patient differ significantly from its structure in a normal person? Was the amyloid the direct cause of Alzheimer's disease? The techniques of molecular biology have apparently produced un­ ambiguous answers to these questions within a very few years. Amyloid is the breakdown product of a large protein ubiquitously produced by a human gene, and there is no significant difference between the gene of an Alzheimer patient and the gene of a normal person. This moves the PAD gene (precursor of Alzheimer's disease A4 amyloid gene) out of the limelight into the rank and file. Yet, there may be surprises in store, if the hint that it is rather close http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Biochemistry Annual Reviews

Molecular Biology of Alzheimer's Disease

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Publisher
Annual Reviews
Copyright
Copyright 1989 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0066-4154
eISSN
1545-4509
DOI
10.1146/annurev.bi.58.070189.001443
pmid
2673012
Publisher site
See Article on Publisher Site

Abstract

SUMMARY AND PERSPECTIVES The amyloid first seen by Alois Alzheimer in the brain of a deceased demented patient (1) turned out to be an extraordinary challenge for biochem­ ists and molecular biologists alike. The extreme insolubility of this polypeptide first challenged the protein chemists attempting to sequence it (2, 3). Then Ithe questions arose: Was the amyloid the product of a slow virus (4) or was it the product of a human gene? If the latter, did the structure of its 0066-4154/0701-0287$02.00 MULLER-HILL & BEYREUTHER gene in an Alzheimer patient differ significantly from its structure in a normal person? Was the amyloid the direct cause of Alzheimer's disease? The techniques of molecular biology have apparently produced un­ ambiguous answers to these questions within a very few years. Amyloid is the breakdown product of a large protein ubiquitously produced by a human gene, and there is no significant difference between the gene of an Alzheimer patient and the gene of a normal person. This moves the PAD gene (precursor of Alzheimer's disease A4 amyloid gene) out of the limelight into the rank and file. Yet, there may be surprises in store, if the hint that it is rather close

Journal

Annual Review of Biochemistry – Annual Reviews

Published: Jul 1, 1989

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