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protein is elevated in late-onset Alzheimer disease families
From the Departments of Neuroscience (N.E.-T., L.H.Y., D.M.Y., M.C.B., M.L.H., S.G.Y.), and Neurology (F.P., N.R.G.-R.), Mayo Clinic Jacksonville, FL; Department of Neurology (N.E.-T.), Mayo Clinic Rochester, MN; and Wisconsin Alzheimer’s Institute and Geriatrics and Gerontology (S.A.), Madison.
* To whom correspondence should be addressed. E-mail: younkin.steve{at}mayo.edu.
ABSTRACT
Objective: Plasma A
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 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 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 
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.
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