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Reiman EM, Quiroz YT, Fleisher AS, Chen K, Velez-Pardo C, Jimenez-Del-Rio M, Fagan AM, Shah AR, Alvarez S, Arbelaez A, Giraldo M, Acosta-Baena N, Sperling RA, Dickerson B, Stern CE, Tirado V, Munoz C, Reiman RA, Huentelman MJ, Alexander GE, Langbaum JB, Kosik KS, Tariot PN, Lopera F. Brain imaging and fluid biomarker analysis in young adults at genetic risk for autosomal dominant Alzheimer's disease in the presenilin 1 E280A kindred: a case-control study. Lancet Neurol. 2012 Dec;11(12):1048-56. PubMed.
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Grand Canyon University
This is fantastic work, but care should be taken not to conflate the common biomarker changes between the Colombian kindred described above and those at risk for late-onset sporadic AD (ApoE4 carriers). In the paper (Valla et al., 2010, cited above), we presented evidence that young adult ApoE4 carriers do not show any amyloid-related changes (increases in soluble amyloid or increased deposition), even though they show functional changes via glucose PET at that age (Reiman et al., 2004, also cited above) and cytochrome oxidase histochemistry. The "common" changes discussed in this article refer to the PET-measured functional changes, not amyloid levels or amyloid deposition. These "common" changes between familial and sporadic AD may be linked by amyloid, but the current evidence suggests they are not.
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