Mutations in the amyloid precursor protein and presenilin 1 and 2 genes result in elevated plasma levels of the amyloid β-peptide species terminating at amino acid residue 42 (Aβ1-42). In a longitudinal study of unrelated elderly individuals, those who subsequently developed Alzheimer's disease had higher plasma levels of Aβ1-42 at entry than did those who remained free of dementia. The results indicate that elevated plasma levels of the released Aβ peptide Aβ1-42 may be detected several years before the onset of symptoms, supporting that extracellular Aβ1-42 plays an important role in the pathogenesis of late-onset Alzheimer's disease.
CITATION STYLE
Mayeux, R., Tang, M. X., Jacobs, D. M., Manly, J., Bell, K., Merchant, C., … Mehta, P. D. (1999). Plasma amyloid β-peptide 1-42 and incipient Alzheimer’s disease. Annals of Neurology, 46(3), 412–416. https://doi.org/10.1002/1531-8249(199909)46:3<412::AID-ANA19>3.0.CO;2-A
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