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Kei Igarashi is a Distinguished Professor in the Department of Cognitive Physiology at Tohoku University Graduate School of Medicine. He earned a B.S. in 2001 and a Ph.D. in 2007 from the University of Tokyo. His postdoctoral training included positions in the laboratory of Kensaku Mori at the University of Tokyo from 2007 to 2009 and in the laboratory of Edvard and May-Britt Moser at the Norwegian University of Science and Technology from 2009 to 2015. He joined the University of California, Irvine as an assistant professor in 2016 and was promoted to Chancellor's Fellow and Associate Professor in the Department of Anatomy and Neurobiology in 2022, where he maintains his primary appointment. In 2025 he was appointed Adjunct Professor at Tohoku University School of Medicine and later named Distinguished Professor there. Igarashi's research examines circuit mechanisms of associative memory in the entorhinal cortex and hippocampus, as well as disruptions of these circuits in Alzheimer's disease models, including the role of dopamine signaling. His laboratory employs in vivo electrophysiological recordings, optogenetics, and behavioral assays in mice. He has received numerous honors, including the Japan Academy Medal and the JSPS Prize in 2023, the Inoue Prize for Science, the BrightFocus Foundation Alzheimer's Disease Research Award in 2019, and earlier awards such as the Mishima Kaiun Prize and the Young Investigator Award from the Japan Neuroscience Society. Selected publications include the 2014 Nature paper on coordination of entorhinal-hippocampal ensemble activity during associative learning, the 2021 Nature paper on dopamine facilitation of associative memory encoding in the entorhinal cortex, and the 2026 Nature Neuroscience paper on early dopamine disruption in a knock-in model of Alzheimer's disease. Igarashi has contributed to editorial and review activities and has delivered invited lectures on memory mechanisms and dementia.
Tohoku University's latest Nature Neuroscience study identifies dopamine disruption in the entorhinal cortex as a core cause of Alzheimer's memory impairment, with restoration via L-DOPA showing promise in mice models.
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