In a new study, researchers have discovered a new class of proteins that protect synapses from being destroyed.
Synapses are the structures where electrical impulses pass from one neuron to another.
The discovery has implications for Alzheimer’s disease and schizophrenia.
If proven, increasing the number of these protective proteins could be a novel therapy for the management of those diseases.
The research was conducted by a team at The University of Texas Health Science Center at San Antonio (UT Health San Antonio).
In Alzheimer’s disease, loss of synapses leads to memory problems and other clinical symptoms. In schizophrenia, synapse losses during development predispose an individual to the disorder.
The team focused on an immune system pathway in the brain that is responsible for eliminating excess synapses; this is called the complement system.
Complement system proteins are deposited onto synapses. They act as signals that invite immune cells called macrophages to come and eat excess synapses during development.
The team discovered proteins that inhibit this function and essentially act as ‘don’t eat me’ signals to protect synapses from elimination.
During development, synapses are overproduced. Humans have the most synapses at the ages of 12 to 16, and from then to about age 20, there is net synapse elimination that is a normal part of the brain’s maturation.
This process requires the complement system.
In adults, synapse numbers are stable, as synapse elimination and formation balance out.
But in certain neurological diseases, the brain somehow is injured and begins to overproduce complement proteins, which leads to excessive synapse loss.
This occurs most notably in Alzheimer’s disease.
In mouse models of Alzheimer’s disease, researchers have found that the removal of complement proteins from the brain protects it from neurodegeneration.
But there was no data to show that there were actually any complement inhibitors in the brain.
The researchers discovered for the first time that there are, that they affect complement activation in the brain and that they protect synapses against complement activation.
One author of the study is Gek-Ming Sia, Ph.D., an assistant professor of pharmacology in UT Health San Antonio’s Long School of Medicine.
The study is published in the journal Nature Neuroscience.
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