Past research has shown that in people at high risk for schizophrenia, abnormal levels of neurotransmitters in the brain tend to be abnormal. However, the scientific community has not yet determined whether these changes occur at the onset of clinically relevant symptoms. People with a type of 22q11.2 deletion syndrome (22q11DS) have a higher risk of Schizophrenia spectrum disorder in adolescence or early adulthood.
Imbalance of neurotransmitters in the brain of chromosomal deletion carriers
This study is mainly aimed at mentally ill patients who carry 22q11 chromosome deletion at the same time, and explores the excitatory/inhibitory neurotransmitter system in their brains before the onset of the disease. Excitatory/inhibitory imbalance occurs in neurotransmitters. In addition, in patients with psychotic symptoms, the concentration of glutamate and glutamine (Glx) in the hippocampal gyrus of the medial temporal lobe of the brain will also increase, and this phenomenon is related to the hippocampus. Back atrophy (Hippocampal atrophy) related.
The research team used a nuclear magnetic resonance spectroscopy called MEGA-PRESS combined with a data analysis software tool called Gannet Toolbox to evaluate the anterior cingulate cortex (Anterior cingulate cortex) of 52 22q11 chromosome deletion carriers and 42 control subjects. , ACC) and the superior temporal cortex (STC), will also measure the concentration of Glx and GABA + in their hippocampus, the latter includes the neurotransmitter γ-aminobutyric acid (γ-aminobutyric acid, GABA), Homocarnosine (Homocarnosine) and other related polymers (collectively known as GABA+).
RESULTS: Although no differences were found in ACC, 22q11 deletion carriers had higher levels of Glx in the hippocampus and STC and lower levels of GABA+ in the hippocampus compared with controls. In addition, the team also found that the concentration of Glx in the hippocampus of chromosomal deletion carriers with psychotic symptoms was significantly higher than that of the control group, and the shrinkage of the hippocampus was significantly related to their elevated Glx levels.
Excessive glutamate release linked to hippocampal shrinkage
Carriers of the 22q11 chromosome deletion have an excitatory/inhibitory imbalance in temporal lobe brain structure, according to findings published today in the medical journal Biological Psychiatry. In subjects with psychotic symptoms associated with hippocampal atrophy, Glx concentrations were further increased in the hippocampal gyrus of the brain. These results are consistent with the theory proposed by the scientific community in the past that abnormally increased glutamate levels can cause excitotoxicity, which in turn causes hippocampal atrophy. The findings underscore the critical role of glutamate in the hippocampus of individuals at genetic risk for schizophrenia and may provide new therapeutic strategies to target glutamate dysfunction and reduce genetic risk risk of developing mental illness.
Further reading: Are teenagers vulnerable to mental illness? The function of brain synapse pruning may be the key!
References:
1. https://www.unige.ch/medecine/psyat/en/research-groups/693eliez/longitudinal-study-22q112-deletion-syndrome/
2. https://pubmed.ncbi.nlm.nih.gov/37011759/
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