A common HIV drug has been shown to improve the connections between memories in aging mice.

The HIV drug maraviroc acts on a cellularprotein known as CCR5 which sits on the surface of white blood cells. maraviroc blocks the entrance if it gets there first.

It does more than that. Researchers working in mouse models found that maraviroc can help the brain after a stroke.

A new mouse study shows that this drug has effects on cells involved in memory. Researchers noticed that the expression of CCR5 in the hippocampus of the mice increased as they aged.

The hippocampus is the hub for memory formation, but a gradual increase in CCR5 expression makes it harder for neurons to link one memory to another.

The researchers found that the group that expressed CCR5 was better at connecting memories that were separated by more time.

The memories were based on fear. The mice were placed in a new context after being taken from their home cage. They were taken to a different place. The animals were taken back to context A to see if they were prepared for a shock after two days.

Within five hours of each other, some mice in the study were introduced to context A and context B. They were introduced to both contexts with a one, two, or seven day separation.

The authors noticed that the rates of freezing in context A were high among regular mice. There was lower freezing among mice with high expressions of CCR5.

When the introductions were separated by two or more days, the mice were unable to link context A to context B.

This temporal window probably exists so that some memories don't link up. It helps us to forget unimportant information if we separated some of them.

Even contexts that are closely related are no longer remembered that way as a mammal ages.

maraviroc reversed the inability to connect context A with context B among older mice. The effects were similar to what was found in mice that were completely knocked out.

The authors write that maraviroc-treated mice showed memory linking.

The memory linking deficits in middle-aged mice can be mitigated by blocking CCR5 with maraviroc. The results show that the temporal window for memory linking is closed by the expression of the CCR5 expression.

If these insights are applicable to humans, then CCR5 could be a useful drug target.

A clinical trial is being planned to test maraviroc's influence on early memory loss in humans.

Alcino Silva from the University of California Los Angeles says that once we fully understand how memory declines, we will have the ability to slow it down.

Nature published the study.