Astrocytes are overloaded with neurons.
Brain cells harvest damaged lipids secreted by hyperactive neurons, then recycle these toxic molecules into energy, scientists report in the January 23, 2019 Janelia Research Campus Medical Center report. cellThis is a mechanism to protect neurons from the harmful side effects of overactivity. And this is another important role for astrocytes that support neurons in different ways.
When a neuron shoots fast and furiously, the lipid molecules in the cell are damaged and can become toxic. While most types of cells emit excess fatty acids or feed them with mitochondria to prevent accumulation, neurons do not rely on these tricks.
Instead, "neurons unload some of the severity of astrocytes," says research co-author and group leader Janelia Zhe Liu, who works closely with Maria Yoanou and Jennifer Lipkinot-Schwarz, senior group leader at Janelia. "People have long suspected that there is such a mechanism, and the new work shows how this process is actually happening."
The find comes from curious observation: Overactive neurons release damaged fatty acids bound to lipid particles. "People do not think that neurons can secrete these lipid particles," Liu says.
But the stimulation of mouse neurons in a dish resulted in fatty acid accumulation and, ultimately, lipid particle release, the team showed. Relative astrocytes then absorb the particles and increase the activity of the genes involved in energy production and detoxification.
Astrocytes nourish neurons from destroyed lipids into their own mitochondria, turning the waste into energy, Liu concluded. Tests in mice show a similar response. After brain damage that mimics a stroke – a huge stress on neurons – neurons increase the production of proteins involved in the transport of fatty acids from the cell and fatty acids accumulated in astrocytes.
This time for cleansing toxic molecules from neurons can be damaged in Alzheimer's patients, Liu says, although this is not fully investigated. The next step, led by Maria Yoanna in her new laboratory at the University of Alberta, is to explore what is different from this mechanism in cell culture and rodent models of Alzheimer's disease.
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Materials provided by Medical Institute Howard Hughes, Note: Content can be edited for style and length.