Gadolinium-based contrast agents have been considered safe for use since 1988 when they were approved by the U.S. Food and Drug Administration. Severe life-threatening side effects usually occur immediately or within 24 hours after application of the contrast agent, and have been reported in a very small number of 0.001-0.01%. Nephrogenic systemic fibrosis (NSF), which can be fatal and is caused by the use of a gadolinium-based contrast agent, was first reported in 2006 in patients with renal failure. Studies have shown that linear contrast agents that have relatively unstable structures and readily release free gadolinium, such as gadodiamide, gadoversetamine, and gimpentetate dimeglumine, are associated with the occurrence of NSF in patients with renal failure. Kanda et al. were the first to report gadolinium deposition in the brain in 2014, almost 8 years after the first report of nephrogenic systemic fibrosis. GBCAs are used in magnetic resonance imaging and serve to enhance the display. They were considered safe if used at the recommended dose. However, following a report confirming that NSF is associated with the use of GBCA in renal patients, evidence has suggested that gadolinium-based contrast agents are not completely eliminated from our body; some GBCAs are deposited in our body, including the brain. Almost all reported studies have confirmed that the deposition of gadolinium in the brain is associated with the chelated structure of the contrast agent since the tendency to deposition was shown by linear contrast agents. This review article aimed to summarize current knowledge and discuss the clinical significance of gadolinium deposition in the brain. Although the number of published articles on this topic is increasing day by day, knowledge about the deposition of gadolinium in the brain is still not enough. There are many unanswered questions and further studies are needed to offer answers.