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Researchers have discovered a previously unknown form of cellular communication in the brain that involves the direct transfer of proteins between neurons. Revealing their findings in the journal Cell Reports, the study authors say that “hijacking this communication” could one day lead to the development of new treatments for dementia and other neurological diseases.
Generally, neuronal communication is mediated by neurotransmitters, which diffuse across synapses in order to relay signals from one cell to the next. However, scientists have also observed the independent movement of certain proteins around the brain, leading to the suspicion that neurons may also be able to correspond by exchanging these compounds.
For example, proteins such as tau and synuclein have been found to move between brain cells and build up into plaques, contributing to the development of Alzheimer’s disease and other neurodegenerative disorders. Until now, though, researchers were unsure if this trans-neuronal transfer of proteins represented a purely pathological mode of communication or if the same mechanism is also involved in healthy brain activity.
To investigate, the study authors used a tagging molecule called biotin to label neuronal proteins in the eyes of rats. Eleven days later, they observed the presence of biotin in neurons within the animals’ visual cortices, indicating that some of the tagged proteins had indeed been transported into distant brain cells.
“This is an entirely new way that cells in the brain can communicate with one another that has never before been integrated into how we think about health and disease,” said study author Dr Hollis Cline in a statement.
Using a technique called mass spectroscopy, the researchers were able to identify roughly 200 tagged proteins that had made the trip to the visual cortex. Importantly, tau and synuclein were both found to be among the transported proteins, indicating that the neuronal transfer of these two compounds is not specific to pathological states.
“This is a confirmation that in the healthy brain, tau and synuclein – and their movement around the brain – is normal,” said Cline. “But with Alzheimer’s disease it’s a toxic form of the protein that is transported between neurons.”
A deeper analysis revealed that the proteins are ferried from one neuron to the next inside membrane-bound packages called exosomes, which mediate cellular communication by carrying an array of messenger compounds between cells. The researchers also found that proteins are typically transferred to excitatory but not inhibitory neurons.
Summarizing the significance of this research, the authors explain that their findings “demonstrate the non-pathological transport of diverse endogenous proteins [between neurons]" and "establish the feasibility of hijacking this communication to manipulate [brain activity]". Much more research will be needed in order to achieve such a feat, although the results of this investigation open up an entirely new avenue for the study and treatment of neurological disorders.
