Fleisher AS, Chen K, Quiroz YT, Jakimovich LJ, Gomez MG, Langois CM, Langbaum JB, Ayutyanont N, Roontiva A, Thiyyagura P, Lee W, Mo H, Lopez L, Moreno S, Acosta-Baena N, Giraldo M, Garcia G, Reiman RA, Huentelman MJ, Kosik KS, Tariot PN, Lopera F, Reiman EM.
Florbetapir PET analysis of amyloid-β deposition in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional study.
Lancet Neurol. 2012 Dec;11(12):1057-65.
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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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