The overall correlation between both sAPPs and Aβ1-42 was relatively weak, and the modest reduction of Aβ1-42 noted in some ADC patients and the opportunistic infections might be secondary to earlier inhibition of the APP pathway and limiting levels of the C-terminal fragment of β-cleaved APP available as substrate for further cleavage by γ-secretase rather than as a result of amyloid plaque deposition as in Alzheimer's disease. Here, APP is linked to early-onset autosomal dominant Alzheimer disease.