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Plasma amyloid β‐peptide 1–42 and incipient Alzheimer's disease
Author(s) -
Mayeux Richard,
Tang MingXin,
Jacobs Diane M.,
Manly Jennifer,
Bell Karen,
Merchant Carol,
Small Scott A.,
Stern Yaakov,
Wisniewski Henry M.,
Mehta Pankaj D.
Publication year - 1999
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/1531-8249(199909)46:3<412::aid-ana19>3.0.co;2-a
Subject(s) - presenilin , pathogenesis , peptide , amyloid (mycology) , alzheimer's disease , extracellular , medicine , disease , dementia , amyloid precursor protein , degenerative disease , amyloid beta , endocrinology , biology , biochemistry , pathology
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.