Publication Date:
1990-06-01
Description:
The amyloid beta peptide (A beta P) is a small fragment of the much larger, broadly distributed amyloid precursor protein (APP). Abundant A beta P deposition in the brains of patients with Alzheimer's disease suggests that altered APP processing may represent a key pathogenic event. Direct protein structural analyses showed that constitutive processing in human embryonic kidney 293 cells cleaves APP in the interior of the A beta P, thus preventing A beta P deposition. A deficiency of this processing event may ultimately prove to be the etiological event in Alzheimer's disease that gives rise to senile plaque formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esch, F S -- Keim, P S -- Beattie, E C -- Blacher, R W -- Culwell, A R -- Oltersdorf, T -- McClure, D -- Ward, P J -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1122-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Athena Neurosciences, Incorporated, South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2111583" target="_blank"〉PubMed〈/a〉
Keywords:
Amino Acid Sequence
;
Amyloid/isolation & purification/*metabolism
;
Amyloid beta-Protein Precursor
;
Humans
;
Molecular Sequence Data
;
Peptide Fragments/isolation & purification
;
Protein Precursors/isolation & purification/*metabolism
;
Protein Processing, Post-Translational/*physiology
;
Transfection
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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