In summary, we can speculate that at earliest stages of AD, discoidal apoA-I-HDL species in plasma, more than alternatively lipidated HDL species, may be involved in synergic activity with brain discoidal apoA-I-HDL pool: the central HDL pool maintains Aβ in a soluble form, while the peripheral HDL pool enhances its efflux from the brain. The gene discussed is APOA1; the disease is Alzheimer disease.