Missing Neurons in Brain’s Social Memory Area Linked to Schizophrenia

Editor's note:

Article originally published in Brain Decoder

By
Kate Baggaley
April 18, 2016

A loss of neurons in part of the hippocampus, a brain region related to memory, might explain some of the symptoms of schizophrenia. Shown in light blue above, this area has long been overlooked because it is so tiny and hard to distinguish from surrounding parts of the hippocampus.

In an experiment, published today in the journal Neuron, scientists found that mice with a rodent version of schizophrenia were missing some of the neurons in this spot, leading to other changes that might account for the problems that those with schizophrenia can have relating to other people.

It's estimated that about 1 percent of adults have schizophrenia, a condition that tends to develop in early adulthood. Schizophrenia is famous for causing hallucinations and delusions, but it also involves social symptoms such as becoming withdrawn and showing an apparent flatness or lack of emotion.

"This is one of the defining features of schizophrenia and it is often present even before the full-blown disease," said coauthor Joseph Gogos, a neuroscientist at Columbia University and the Zuckerman Institute in New York City. "Part of it is linked to impaired social cognition, a mental operation that allows us to perceive the intent, the mood and the action of other people and respond appropriately."

Postmortem examinations on people who had schizophrenia have revealed that their neurons were diminished in a spot in the hippocampus called area CA2. This brain region helps us form memories of social interactions.

To investigate how an altered CA2 region might contribute to the disease, Gogos and his colleagues genetically engineered mice to have symptoms resembling those of schizophrenia. Specifically, they replicated a genetic deletion that has been found in subsets of people with a high risk of developing schizophrenia and similar disorders.

As the altered mice reached adulthood, they started to show symptoms of faulty social cognition. The rodents spent a long time investigating mice they had already met, indicating that they could not recall previous encounters.

A brain tissue examination of these mice showed the rodents had fewer neurons in area CA2 than their healthy peers did, leading to alterations in the activity and connections among the remaining neurons.

These changes—the loss of neurons and social symptoms— emerged as the mice entered young adulthood, which parallels the onset of schizophrenia in people, Gogos said.

"How might these changes lead to impaired social memory, we do not know but it is our intention to understand this," said Gogos. "Part of the explanation may have to do with the fact that CA2 contains high levels of vasopressin, a hormone that plays a role in social behaviors."