Microglia—specialized immune cells of the central nervous system—are thought to play a role in causing neurodevelopmental and neuropsychiatric conditions such as autism spectrum disorders, schizophrenia, bipolar disorder, and psychosis. The protein Iba1 is a well-known marker for microglia, yet its function in the brain has never been uncovered.

In a study published online on November 16 in Proceedings of the National Academy of Sciences of the United States of America, Sayan Nandi, Ph.D., Pablo Castillo, M.D., Ph.D., and Nicholas Sibinga, M.D., and colleagues describe Iba1’s role in the healthy brain. Using mice in which the gene coding for Iba1 was deleted, the researchers showed that Iba1’s absence leads to structural and functional impairments in microglia that significantly affect synaptic development and behavior. Specifically, synapse formation was reduced, and this deficit persisted into adulthood. Impairments in object recognition memory and social interaction were also observed. The findings suggest that modifying microglial function could help in treating certain neurodevelopmental and neuropsychiatric disorders.

Dr. Nandi is a research assistant professor of developmental & molecular biology at Einstein (R21 NS116480 and R21 MH124294). Dr. Castillo is a professor of psychiatry and behavioral sciences, and in the Dominick P. Purpura Department of Neuroscience, as well as the Harold and Muriel Block Chair in Neuroscience at Einstein (R01 MH125772, R01 MH116673, and R01 NS113600). Dr. Sibinga is a professor of medicine and of developmental and molecular biology at Einstein (R01 HL128066 and R01 HL133861). The first author of the study is Pablo Lituma, a former Ph.D. student in the Dominick P. Purpura Department of Neuroscience (F31MH109267).