Lefterov et al. demonstrated that both lipidated and non-lipidated apoA-I attenuated Aβ42 aggregation and toxicity in primary brain cells, and further showed that while apoA-I deficiency did not affect APP processing and soluble/insoluble brain parenchyma Aβ levels, 12-month-old APP/PS1 mice lacking apoA-I had higher insoluble Aβ levels in cerebral blood vessels and memory deficiencies (Lefterov et al., 2010). The gene discussed is APOA1; the disease is memory.