In the brain, a polymorphism in the APOCI allele that leads to an increase in APOCI expression has been implicated as a risk factor in the pathogenesis of Alzheimer’s disease (AD) [12–14]; consistently, expression of human APOCI in mice can lead to learning and memory impairment, perhaps as a result of alterations in brain lipid metabolism or by interfering with ApoE binding to β-amyloid peptides [12, 13, 15, 16]. Here, APOC1 is linked to early-onset autosomal dominant Alzheimer disease.