In 2016, Dr. Siegelbaum and fellow Zuckerman Institute Principal Investigator Joseph Gogos, MD, PhD, found that mice carrying a human mutation linked to schizophrenia have a dysfunctional CA2. This provided striking evidence that social memory deficits, a key feature of schizophrenia, may have their origins in CA2.
“People with schizophrenia exhibit a wide range of behavioral alterations, including impaired social memory and altered levels of aggression,” said Dr. Siegelbaum. “Might this result from a loss or change in CA2 activity? And could these deficits be alleviated by artificially boosting CA2 activity? That is something that our research, and that of others, hopes to reveal.”
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