Led by UK DRI Centre Director Giles Hardingham, a group of researchers at The University of Edinburgh have uncovered mechanisms involved in the protection of nerve cells - called neurons - in the brain, offering hope in the future for potential new ways to treat dementias.
It has been known for over 30 years that when neurons are active, certain genes are turned on. These genes are important for neurons to develop and mature, as well as for learning, memory, and even survival of neurons in adults. However, in the human brain the number of neurons is at least matched by the number of other cells - called glia - which play crucial roles in the survival and support of neurons.
Until now, how and if neurons control gene expression in glia was completely unknown.
In new work published today in Nature Communications, Professor Hardingham’s group showed that neurons do in fact control the expression of hundreds of genes in particular glial cells called astrocytes. They found that neurons controlled the expression of astrocytic genes that are essential for the neurons themselves to pass messages to one another. Additionally, it was discovered that when neurons were active they turned on astrocytic genes leading to increased antioxidant and nutritional support of neurons.
The group in Edinburgh went on to find that such neuro-protective genes were turned down in astrocytes in neurodegenerative disease and ageing. These results shine a new light onto how the ability of glia to protect neurons may become impaired in dementia, giving hope for a potential new route for treatment.
Professor Hardingham said, "The capacity of astrocytes to protect and support nearby neurons is one of the reasons that the human brain can function for many decades, and their impairment is a likely contributor to brain malfunction in dementias.
"Now we know have uncovered the signal pathways that control the neuro-protective genes in astrocytes, our next step is to try to artificially manipulate these pathways to boost the capacity of astrocytes to protect neurons, which may validate these pathways as potential therapeutic targets."
