Abstract |
Mutations in the amyloid precursor protein and presenilin 1 and 2 genes result in elevated plasma levels of the amyloid beta-peptide species terminating at amino acid residue 42 (A beta1-42). In a longitudinal study of unrelated elderly individuals, those who subsequently developed Alzheimer's disease had higher plasma levels of A beta1-42 at entry than did those who remained free of dementia. The results indicate that elevated plasma levels of the released A beta peptide A beta1-42 may be detected several years before the onset of symptoms, supporting that extracellular A beta1-42 plays an important role in the pathogenesis of late-onset Alzheimer's disease.
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Authors | R Mayeux, M X Tang, D M Jacobs, J Manly, K Bell, C Merchant, S A Small, Y Stern, H M Wisniewski, P D Mehta |
Journal | Annals of neurology
(Ann Neurol)
Vol. 46
Issue 3
Pg. 412-6
(Sep 1999)
ISSN: 0364-5134 [Print] United States |
PMID | 10482274
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Amyloid beta-Peptides
- Peptide Fragments
- amyloid beta-protein (1-43)
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Topics |
- Age of Onset
- Aged
- Aged, 80 and over
- Alzheimer Disease
(blood)
- Amyloid beta-Peptides
(blood)
- Female
- Humans
- Male
- Odds Ratio
- Peptide Fragments
(blood)
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