Journal
NEUROLOGY
Volume 70, Issue 8, Pages 596-606Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/01.wnl.0000278386.00035.21
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Funding
- NIA NIH HHS [F32 AG020903-02, AG16574, F32 AG020903, AG18023, AG06656] Funding Source: Medline
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Objective: Plasma A ss 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 A ss 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 A ss 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 epsilon 4 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 A ss.
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