Alzheimer disease (AD) is the most common cause of progressive cognitive dysfunction in our community. The link between its clinical manifestations—progressive learning and memory impairments and mounting deficits in other cognitive domains—and the cortical deposition of Aβ-amyloid plaques and tau-rich neurofibrillary tangles/neurites has been well established. As our population ages and dementia syndromes become more commonplace, there is increasing interest in the use of biomarkers during life to assist in confirming, or excluding, AD. The obvious benefits for such biomarkers are many: patient and clinician certainty, exclusion of atypical or reversible dementia syndromes, and the identification of preclinical and prodromal participants appropriate for disease-modification trials.
