New brain neural circuits and genes responsible for learning, memory, and cognitive functions have been identified.
The Korea Research Foundation announced early December that a joint research team, including Shim In-seop, a medical professor at Kyung Hee University, and Kim Chul-hee, a professor at Chungnam National University, has found a new gene (GNG8) and a neural circuit related to cognitive and developmental disorders and brain diseases.
The research team previously had found that if the “Samdol” gene is not expressed in the brain’s habenular nucleus, it can lead to autism. “Samdol” is a cytokine gene expressed in the nervous system, known as a key factor related to mental illness, especially autism. In order to find out the details, the research team tried to find a new gene that is uniquely expressed in the brain’s habenular nucleus.
As a result, the team discovered the gene GNG8, associated with cognitive impairment.
The habenular nucleus, which has GNG8, is deemed to be involved in emotional control, such as emotions, hatred, and sleep. However, its relevance to cognitive functions is unknown.
The research team confirmed that cognitive disorders appear in the mice which lost the GNG8 gene with actual gene scissors technology. Manual avoidance tests and underwater labyrinth tests showed abnormalities to long-term memory and space learning. The fact that the lack of GNG8 led to significant degradation of learning, memory, and cognitive functions was confirmed by the genetically defective mouse model.
Furthermore, the research team found that this cognitive degradation was the result of reduced acetylcholine production in the brain’s habenular nucleus. Less acetylcholine or fewer cholesterol nerve cells in the brain lead to decreased cognitive function. In fact, acetylcholinease inhibitors are being used to ease memory damage of Alzheimer’s dementia.
Compared to normal mice, mice without GNC8 produced significantly fewer neurotransmitters, acetylcholine and its synthetics, which regulate memory and learning, and significantly reduced long-term reinforcement (LTP), a brain synaptic plasticity indicator associated with learning and memory.
When a compound was administered that strengthened acetylcholine signal transmission, long-term memory and spatial learning disorders were recovered.
As the research revealed new brain neural circuits and genes responsible for learning and memory, it is expected to serve as the basis for research into the development of treatments for cognitive memory and neurodegenerative diseases targeting them.
The results of the study were published on September 28 in the international journal “Molecular Psychiatry.”
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