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Abstract
Objective: Plasma Aβ levels are elevated in early-onset Alzheimer disease (AD) caused by autosomal dominant mutations. Our objective was to determine whether similar genetic elevations exist in late-onset AD (LOAD).
Methods: We measured plasma Aβ in first-degree relatives of patients with LOAD in a cross-sectional series and in extended LOAD families. We screened these subjects for pathogenic mutations in early-onset AD genes and determined their ApoE genotypes.
Results: Plasma Aβ is significantly elevated in the LOAD first-degree relatives in comparison to unrelated controls and married-in spouses. These elevations are not due to ApoE ε4 or pathogenic coding mutations in the known early-onset AD genes.
Conclusions: The findings provide strong evidence for the existence of novel, as yet unknown genetic factors that affect late-onset Alzheimer disease by increasing Aβ.
Glossary
- AD=
- Alzheimer disease;
- COV=
- coefficient of variation;
- ELISA=
- enzyme-linked immunosorbent assay;
- EOFAD=
- early-onset familial AD;
- IDE=
- insulin-degrading enzyme;
- LOAD=
- late-onset AD;
- MMSE=
- Mini-Mental State Examination;
- NGR=
- neurology examination;
- RFLP=
- restriction fragment length polymorphism.
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