Treatment development in Alzheimer disease (AD) has been systematically moving to earlier stages of disease to target prodromal and even preclinical stages of AD, thereby changing treatment into prevention. Given our increasing understanding of the neurobiologic mechanisms underlying early AD, the hope is to use biomarkers to target treatments to persons who have the greatest risk of developing AD. The most promising of these biomarkers to date is amyloid brain burden quantified either by amyloid–positron emission tomography (PET) or cerebrospinal fluid assays. But these biomarkers are innately invasive and/or expensive and unlikely to be practical in large-scale population screening. For these reasons, investigators have been seeking low-cost methods of screening, including more sensitive cognitive tests1 and subjective report of memory complaints.2 It has been increasingly clear that AD affects more than just cognition and that neuropsychiatric symptoms in cognitively healthy older adults may be prodromal symptoms of AD.3,4 This concept has been termed mild behavioral impairment5 as a parallel concept to mild cognitive impairment.