One factor that determines how at risk an individual is of developing late-onset Alzheimer disease (AD) is the version of the APOE gene that they carry — those carrying the gene that enables them to make the apoE4 form of the apoE protein are at increased risk and those carrying the gene that enables them to make the apoE2 form are at decreased risk. It has been hypothesized that increasing the amount of lipid (fat) associated with apoE by overexpressing the protein ABCA1 might decrease amyloid deposition in the brain, the hallmark of AD. Evidence to support this hypothesis has now been generated in mice by David Holtzman and colleagues at Washington University School of Medicine, St Louis.
