In addition to extracellular deposition of β-amyloid (Aβ) plaques, Alzheimer disease (AD) is defined by the intracellular aggregation of tau in neurofibrillary tangles (NFTs), composed of abnormally hyperphosphorylated tau.1 Tau pathology is thought to be reflected in CSF levels of phosphorylated tau (p-tau). The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.