Publication Date:
1987-02-20
Description:
The amyloid beta protein has been identified as an important component of both cerebrovascular amyloid and amyloid plaques of Alzheimer's disease and Down syndrome. A complementary DNA for the beta protein suggests that it derives from a larger protein expressed in a variety of tissues. Overexpression of the gene in brain tissue from fetuses with Down syndrome (trisomy 21) can be explained by dosage since the locus encoding the beta protein maps to chromosome 21. Regional localization of this gene by both physical and genetic mapping places it in the vicinity of the genetic defect causing the inherited form of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanzi, R E -- Gusella, J F -- Watkins, P C -- Bruns, G A -- St George-Hyslop, P -- Van Keuren, M L -- Patterson, D -- Pagan, S -- Kurnit, D M -- Neve, R L -- AG00029/AG/NIA NIH HHS/ -- HD10658/HD/NICHD NIH HHS/ -- HD20118/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):880-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2949367" target="_blank"〉PubMed〈/a〉
Keywords:
Alzheimer Disease/*genetics
;
Amino Acid Sequence
;
Amyloid/*genetics
;
Amyloidosis/genetics
;
Brain/physiopathology
;
Chromosome Mapping
;
*Chromosomes, Human, Pair 21
;
DNA/genetics
;
Down Syndrome/genetics
;
Gene Expression Regulation
;
Genetic Linkage
;
Humans
;
RNA, Messenger/genetics
;
Tissue Distribution
;
Transcription, Genetic
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
Permalink
