Open University Interactive Learning: The Real Wonder Woman

Click on the image to visit the Open University site and run the interactive presentation.

The women portrayed in this interactive are just a selection of influential, pioneering and successful women from across the world.

They were chosen for their remarkable contributions to their field, despite their educational, social and economic status.

Many were trailblazers for future women working in male-dominated fields; many had to fight for success and recognition which may have gone ignored.

While this list is by no means exhaustive, we hope it inspires you to celebrate the importance of women's achievements and to learn from their stories.

Gardening in the Brain: Cells Called Microglia Prune the Connections Between Neurons

Microglia (green) in a mouse brain. The nuclei of all cells in the brain are labelled blue. (Credit: EMBL/R. Paolicelli)

Gardeners know that some trees require regular pruning: some of their branches have to be cut so that others can grow stronger.

The same is true of the developing brain: cells called microglia prune the connections between neurons, shaping how the brain is wired, scientists at the European Molecular Biology Laboratory (EMBL) in Monterotondo, Italy, discovered. Published online in Science, the findings could one day help understand neurodevelopmental disorders like autism.

"We're very excited, because our data shows microglia are critical to get the connectivity right in the brain," says Cornelius Gross, who led the work: "they 'eat up' synapses to make space for the most effective contacts between neurons to grow strong."

Microglia are related to the white blood cells that engulf pathogens and cellular debris, and scientists knew already that microglia perform that same clean-up task when the brain is injured, 'swallowing up' dead and dying neurons.

Looking at the developing mouse brain under the microscope, Gross and colleagues found proteins from synapses -- the connections between neurons -- inside microglia, indicating that microglia are able to engulf synapses too.

To probe further, the scientists introduced a mutation that reduced the number of microglia in the developing mouse brain.

"What we saw was similar to what others have seen in at least some cases of autism in humans: many more connections between neurons," Gross says. "So we should be aware that changes in how microglia work might be a major factor in neurodevelopmental disorders that have altered brain wiring."

The microglia-limiting mutation the EMBL scientists used has only temporary effects, so eventually the number of microglia increases and the mouse brain establishes the right connections.

However, this happens later in development than it normally would, and Gross and colleagues would now like to find out if that delay has long-term consequences.

Does it affect the behaviour of the mice behaviour, for example? At the same time, Gross and colleagues plan to investigate what microglia do in the healthy adult brain, where their role is essentially unknown.

Gene switch rejuvenates failing mouse brains

Gene switch rejuvenates failing mouse brains

Step aside, Sudoku. A genetic switch that causes memory impairment in ageing mice when it goes into "off" mode has been flicked on, restoring failing brains to a more youthful state.

If a similar switch can be found in people, it might provide a new way to keep ageing human brains young.
Cognitive decline, particularly memory impairment, is a normal part of ageing in humans and animals. Yet why this happens, and how we can prevent it, is largely unknown, says David Sweatt at the University of Alabama, Birmingham, who was not involved in the new work.

André Fischer of the European Neuroscience Institute in Göttingen, Germany, and colleagues forced 3-month-old mice to find their way around a new environment and assessed them on their ability to associate an electric shock with a particular environment.

New neurons
The result was increased activity of a cluster of over 1500 genes which are known make proteins that are needed for the creation of new neurons – a process that is necessary for learning in humans and mice.

This boost in gene expression did not occur in 16-month-old mice given the same tasks: the activity of their genes changed only slightly. The mice also did worse than the young ones at spatial learning and memory tasks.

To uncover what prevents elderly mice getting this genetic boost, Fischer analysed the DNA found in neurons in the hippocampus of both old and young mice.

They found that when young mice are learning, a molecular fragment known as an acetyl group binds to a particular point on the histone protein that DNA wraps itself around – with the result that the cluster of learning and memory genes on the surrounding DNA ends up close to the acetyl group.

DNA 'on' switch
This acetyl "cap" was missing in the older mice that had been set the same tasks. From this, the team concludes that the cap acts as an "on" switch for the cluster of learning and memory genes: removing the cap switches off the genes.

Next, by injecting an enzyme known to encourage caps to bind to any kind of histone molecule, Fischer's team artificially flipped the switch to the on position in old mice. The acetyl group returned to the histone molecule and the mice's learning and memory performance became similar to that of 3-month-old mice.