Protein study shows how our brain forms memories

Studies conducted on a protein called kibra shows how our brain creates and erases memories. Scientists from John Hopkins University used a mouse model where they decreased the amount of kibra in the brain, and showed that animals lacking this protein showed less plasticity, which basically means neurons were less able to make new connections and disconnect from other neurons. This process is highly important in the formation of memories, as they consist of various connections between neurons, linking factors such as smell, vision, taste and other parameters into one cohesive image of the past. The kibra study gives us more insight into the highly complex process of memory formation, and might aid us in developing methods to counter neurodegenerative diseases in which the memory function of the brain is altered, such as Alzheimer's disease.

Mechanistically, kibra was found to be associated with so called AMPA receptors. These receptors need to be transported from inside the neuron to a communication junction that is called the synapse. This is where communication between neurons take place, and connections can be established. AMPA receptors are constantly taken to the synapse and correspondingly recycled, after their job in communicating with other neuronal cells is done. Mice lacking kibra were found to have slower transport of AMPA receptors, impairing their ability to form new connections. In mice that had no functional kibra at all, serious defects in learning and memory were found.

Neurons posses a long 'tail', called an axon, which they are able to grow and allows them to connect to others. After arriving at a neigbouring neuron, the synapse is established, and chemical communication by so called neurotransmitters is established. Receptors are needed to collect the chemical signals on the other side of the junction, which is called the dendrite. All neurons posses an axon to connect to other neurons, while they have a big network of dendrites with receptors to receive incoming connections from others. While the amount of axons per neuron is limited to one, the length can be extraordinary: the longest axon, from the sciatic nerve, runs from the base of the spine all the way to the big toe.

The interaction between kibra, AMPA receptors and the neuronal synapse reveals a basic mechanism by which the brain works to form memories. While the functional mechanism of kibra has only been assessed in mice, it was already linked to memory function in humans. As we seem to share the way of forming memories with mice, the study might give rise to new therapies to counter degradation of memory function in humans. Kibra, along with other molecules that have an effect in the AMPA recycling pathway, may protect us against memory impairment due to neurodegenerative diseases. In fact, kibra has already been linked to protection against Alzheimer's disease, though functional analysis remains to be performed.