Cited by 434Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Plasma Aβ40 and Aβ42 and Alzheimer’s disease: Relation to age, mortality, and risk

Mayeux, R., Honig, L. S., Tang, M.-X., Manly, J., Stern, Y., Schupf, N., Mehta, P. D.·2003·Neurology

Abstract

BACKGROUND: Plasma amyloid [beta]-peptide (A[beta]) 40 and A[beta]42 levels are increased in persons with mutations causing early-onset familial Alzheimer's disease (AD). Plasma A[beta]42 levels were also used to link microsatellite genetic markers to a putative AD genetic locus on chromosome 10 and were observed in patients with incipient sporadic AD. METHODS: The authors measured plasma A[beta]40 and A[beta]42 levels using a sandwich ELISA after the initial examination of 530 individuals participating in an epidemiologic study of aging and dementia. Participants were examined at 18-month intervals, and plasma A[beta]40 and A[beta]42 levels were repeated in 307 subjects 3 years after baseline. RESULTS: Compared with individuals who never developed AD, patients with AD at baseline and those who developed AD during the follow-up had significantly higher A[beta]42, but not A[beta]40, plasma levels. The risk of AD in the highest quartile of plasma A[beta]42 was increased by more than twofold over that in the lowest quartile. The highest plasma A[beta]42 levels were observed in patients with AD who died during the follow-up. Plasma A[beta]42, but not A[beta]40, levels decreased over time in patients with newly acquired AD. CONCLUSIONS: Plasma A[beta]40 and A[beta]42 increase with age and are strongly correlated with each other. Plasma A[beta]40 and A[beta]42 levels are elevated in some patients before and during the early stages of AD but decline thereafter. High plasma A[beta]42 levels may also be associated with mortality in patients with AD.

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Crossref · 10.1212/01.wnl.0000091890.32140.8f

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Authors
Mayeux, R., Honig, L. S., Tang, M.-X., Manly, J., Stern, Y., Schupf, N., & Mehta, P. D.
Affiliations
Columbia University Irving Medical Center (US)
Venue
Neurology
Published
2003-11-11
Volume
61
Issue
9
Pages
1185-1190
ISSN
  • 0028-3878 (ISSN-L)
  • 1526-632X
OpenAlex
W2065184319
Cited by
434
References
45
Citations by year
2026: 6 · 2025: 13 · 2024: 12 · 2023: 10 · 2022: 6 · 2021: 17 · 2020: 16 · 2019: 13 · 2018: 11 · 2017: 19 · 2016: 18 · 2015: 24 · 2014: 23 · 2013: 19 · 2012: 29
FWCI
10.95
Type
journal article
Language
en
Open access
closed
Locations
  • Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute on Aging (AG08702, P01AG007232, AG 07232, P50AG008702)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, Aβ40, amyloid-beta 42, plasma biomarkers, early-onset familial Alzheimer's disease, sporadic Alzheimer's disease, dementia risk, disease progression, mortality, aging
MeSH terms
Age Factors, Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Female, Follow-Up Studies, Humans, Lipids, Male, Neuropsychological Tests, New York City, Peptide Fragments, Predictive Value of Tests, Body Mass Index, Multivariate Analysis, Proportional Hazards Models, Amyloid beta-Peptides, Age Distribution, Risk Assessment

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