Alzheimer’s disease (AD), a serious degenerative disease of the central nervous system, is the most common cause of dementia in the elderly. Its etiology has not yet been elucidated. ATP-binding cassette transporter A7 (ABCA7) has a high level expression in the brain. Since the genome-wide association studies identified ABCA7 as a risk gene for AD, more and more evidence from in vitro, in vivo, and human-based studies has confirmed that ABCA7 is one of the most important risk genes for early-onset and late-onset AD. ABCA7 mediates phospholipid efflux and its distribution in neurons, and plays a weak but significant role in cholesterol regulation, so as to maintain the lipid homeostasis in the brain. ABCA7 is also closely related to microglia phagocytosis and immune function. When lipid homeostasis in the brain is unbalanced or ABCA7 is defective, it will reduce the ability of microglia to process Aβ, causing abnormal accumulation of Aβ and triggering the inflammatory response in the brain. ABCA7 single nucleotide polymorphism (SNP) variants or loss-of-function (LOF) mutations are also significantly associated to the risk of AD. We suggest that ABCA7 may be a potential biomarker or therapeutic target for early detection and diagnosis of AD. In this paper, the role of ABCA7 in the occurrence and development of AD is reviewed, in order to provide therapeutic ideas for the clinical prevention and treatment of AD.