Role of Family History for Alzheimer Biomarker Abnormalities in the Adult Children Study

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Abstract
Recent advances suggest that Alzheimer disease (AD) has a lengthy period in which cerebral lesions gradually accumulate in the absence of symptoms, eventually causing sufficient synaptic and neuronal damage to result in symptomatic AD.1-5 Since 2005, Antecedent Biomarkers for AD: The Adult Children Study (ACS) has enrolled a cohort of cognitively normal 43- to 76-year-old individuals in an extensive study of biomarkers for AD before its symptomatic stages. In addition to clinical and cognitive measures, a broad spectrum of candidate antecedent biomarkers for AD were assessed, including magnetic resonance imaging (MRI)–based brain volumes, diffusion tensor imaging–based measures of white matter microstructure, cerebrospinal fluid (CSF), and molecular imaging of cerebral fibrillar amyloid with positron emission tomography (PET) using the [11C] benzothiazole tracer, Pittsburgh compound B (PIB). Because the ACS cohort is cognitively normal, changes in these well-established biomarkers for AD likely represent the insidious pathogenesis of AD well before the development of symptoms, ie, during the preclinical stage of AD.