For the first time, researchers have uncovered the mechanism behind adult brain plasticity. Ultimately, their findings could lead to the development of new strategies in the treatment of neurological disorders.
In its developmental phase, as it learns and registers new information, the brain constantly causes new neural connections to emerge. He maintains and reinforces data teaching him, for example, how to avoid a danger while the connections deemed useless are pruned. Adult brains work the same way, but scientists still didn’t know how the “unnecessary connections” were eliminated in this case. Till today. According to a study published on December 23 in the journal Nature, researchers have uncovered the mechanism behind this plasticity and possibly the neurological disorders that affect hundreds of millions of people worldwide.
In the brain, gray matter contains microglia and astrocytes, two complementary cells that support neurons and synapses in particular. Microglia are an essential immune defense that consume pathogens and dead cells, while astrocytes are star-shaped cells that help structure the brain and maintain homeostasis by participating in the control of signaling between cells. neurons.
Until then, researchers thought that the microglial ate up the synapses while performing its cleaning. This process is called phagocytosis. But, “using new tools, we show that, for the first time, it is astrocytes and not microglia that consistently eliminate excess and unnecessary adult excitatory synaptic connections in response to neuronal activity,” he said. professor the author of the article, Won-Suk Chung, assistant professor at the department of biological sciences of KAIST (South Korea).
An article that “challenges the general consensus”
He and his collaborators thus developed a molecular sensor to detect the elimination of synapses by glial cells and calculated the frequency and type of cellular synapses eliminated. They also used it on adult mice lacking the gene allowing astrocytes to eliminate synapses. They were thus able to notice that animals with defective astrocytic phagocytosis had many more excitatory synapses in the hippocampus. The researchers then realized that they were modified, causing impaired learning and memory in rodents lacking the famous gene.
“Through this process, we show that, at least in the CA1 region of the adult hippocampus, astrocytes are the primary players in synapse removal, and this astrocyte function is essential for controlling synapse number and plasticity.” , explains Won-Suk Chung.
“Our article challenges the general consensus in this field that microglia are the primary synapse phagocytes that control the number of synapses in the brain,” he continues.
A new strategy in the treatment of brain disorders?
This is why, “our findings have profound implications for our understanding of how neural circuits change during learning and memory, as well as in disease”, says the researcher. “Changes in the number of synapses are strongly associated with the prevalence of various neurological disorders, such as autism spectrum disorders, schizophrenia, frontotemporal dementia, and several forms of seizures.”
In the long term, researchers want to understand how the renewal of synapses by astrocytes affects neurological disorders. “It is intriguing to postulate that modulating astrocyte phagocytosis to restore synaptic connectivity could be a novel strategy in the treatment of various brain disorders,” Chung concludes.
Neurological disorders are afflictions of the central or peripheral nervous system. They affect the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction and muscles.
Among them, WHO account “epilepsy, Alzheimer’s disease and other dementias, cerebrovascular diseases including stroke, migraine and other headaches, multiple sclerosis, Parkinson’s disease, infections of the nervous system, brain tumours, traumatic disorders of the nervous system such as head trauma, and neurological disorders related to malnutrition”.
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