Autor: |
Mayeux R; Taub Alzheimer's Disease Research Center, Staten Island, NY, USA., Tang MX, Jacobs DM, Manly J, Bell K, Merchant C, Small SA, Stern Y, Wisniewski HM, Mehta PD |
Jazyk: |
angličtina |
Zdroj: |
Annals of neurology [Ann Neurol] 1999 Sep; Vol. 46 (3), pp. 412-6. |
DOI: |
10.1002/1531-8249(199909)46:3<412::aid-ana19>3.0.co;2-a |
Abstrakt: |
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. |
Databáze: |
MEDLINE |
Externí odkaz: |
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