Researchers at the University of Texas have identified a new subset of proteins capable of protecting synapses- the structures neurons use to communicate- from being destroyed. As synapse loss is a known contributing factor towards Alzheimer's disease and schizophrenia, the findings may inform new therapeutics.
Loss of synapses is partially responsible for memory problems in Alzheimer's. Meanwhile, synapse losses during brain development make one more susceptible to schizophrenia.
As children grow up, they overproduce synapses, reaching their peak number of synapses somewhere between the ages of 12 and 16. Then, between ages 16 and 20, the brain undergoes net synapse elimination as a normal part of the maturation process.
Once in adulthood, synapse numbers stabilize, being formed and destroyed at roughly the same rate. However, in some neurological diseases, the brain overproduces complement proteins, which signal immune cells called macrophages to essentially eat synapses. This leads to excessive synapse loss and is a notable occurrence in Alzheimer's disease.
In their research, the scientists discovered proteins that prevent this function and essentially act as 'don't eat me' signals that protect synapses from being destroyed. This follows previous studies finding that the removal of complement proteins from mice leads to protection against neurodegeneration.
"We've known about the complement proteins, but there was no data to show that there were actually any complement inhibitors in the brain," says Dr Gek-Ming Sia, a senior author of the research. "We discovered for the first time that there are, that they affect complement activation in the brain, and that they protect synapses against complement activation."
Dr. Sia continued that the findings could explain why there is a preferential loss of specific synapses in certain diseases, and why some people are more susceptible to synapse loss.
In future research, the researchers aim further study how much complement system biology can explain the development of psychiatric disorders, how the number of compliment inhibitors could be altered, and if this would have any clinical effects. They also want to know whether different neurons produce different compliment inhibitors capable of protecting different synapse subsets.