In:
Science, American Association for the Advancement of Science (AAAS), Vol. 248, No. 4959 ( 1990-06), p. 1122-1124
Abstract:
The amyloid β peptide (AβP) is a small fragment of the much larger, broadly distributed amyloid precursor protein (APP). Abundant AβP 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 AβP, thus preventing AβP 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.
Type of Medium:
Online Resource
ISSN:
0036-8075
,
1095-9203
DOI:
10.1126/science.2111583
Language:
English
Publisher:
American Association for the Advancement of Science (AAAS)
Publication Date:
1990
detail.hit.zdb_id:
128410-1
detail.hit.zdb_id:
2066996-3
SSG:
11
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