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Schizophrenia causes, among other things, hallucinations and problems of memory or cognition. This psychiatric illness affects 0.5% of the general population and could be related to genetic abnormalities of chromosome 22, known as 22q11 deletion syndrome. However, not all people with the syndrome develop psychotic symptoms. So, what triggers the disease? Researchers at the University of Geneva (UNIGE) in Switzerland provided an initial response after observing and badyzing several years of patients with deletion syndrome.
Scientists found that the size of the hippocampus, the region of the brain responsible for memory and emotions, was smaller than normal but followed the same developmental curve as in healthy subjects. Yet when the first psychotic symptoms appear – usually in adolescence – the hippocampus will atrophy dramatically. The results, which you can read in the newspaper Molecular Psychiatry, open new ways to understand the causes of schizophrenia.
22q11 deletion syndrome is a neurogenetic disorder that targets chromosome 22. Thirty percent of those affected by the syndrome develop schizophrenia-specific psychotic symptoms, such as auditory hallucinations, memory problems, disorders affecting their perception of the reality and difficulties of social interactions characterized by strong paranoia. "We now know that schizophrenia is linked to the hippocampus, a complex area of the brain that performs a multitude of processes simultaneously related to memory, imagination, and emotions," says Stephan Eliez, professor at Department of Psychiatry of the Faculty of UNIGE. of medicine. Recent studies have shown that people with deletion syndrome have a smaller than average hippocampus. "That's why we studied the development of this structure in detail," continues the researcher at UNIGE, "so we can understand why some people with deletion syndrome eventually develop psychotic symptoms, so than others no. "
18-year study on the development of the hippocampus
The Geneva team follows 275 patients aged 6 to 35 years old for 18 years: a control group of 135 people – that is to say, people without genetic problems – and 140 people with deletion syndrome, including 53 with moderate to severe psychotic symptoms.
They underwent an MRI every three years so that we can observe their brain development. This helped us to create a statistical model that measures and compares the evolution of the hippocampus in both groups of patients. "
Valentina Mancini, researcher in the Department of Psychiatry at UNIGE
It was found that the hippocampus of the deletion syndrome group, although smaller from the beginning, followed a growth pattern identical to that of the control group. "This meant that we could hypothesize that the smallest size of the hippocampus originates in utero during its development in the uterus."
UNIGE scientists also observed in detail the subfields of the hippocampus, discovering that one of them – called CA3 – was not affected by size reduction. "This subfield plays a crucial role in the work of memorization and seems stronger than the other sub-parts," adds Professor Eliez.
Adolescence: the period that matters most
The researchers then compared the developmental curves of the hippocampus in people with deletion syndrome but exhibiting no psychotic symptoms with those having developed psychotic symptoms. "There is no doubt about our results: around 17 or 18 years, people with schizophrenic symptoms undergo a radical atrophy of the size of their hippocampus, and particularly in the CA3 zone, although CA3 initially succeeded to develop normally, unlike the other subfields, "says Mancini. But why?
Researchers do not yet have a precise answer that can explain the drastic fall in the development of this vital structure of the brain. But their badumptions are focused on environmental factors, such as neuronal stress or inflammation. "The hippocampus of people with deletion syndrome is smaller, it means that it has to compensate for its size by hyperactivity .In case of huge stressor, especially during the critical period of In adolescence, this hyperactivity could lead to a significant increase in glutamate. " this "poisons" the hippocampus and causes its atrophy, "says Mancini.Psychotic symptoms can result from this hyper-compensation, which eventually destroys the hippocampus.
Act before the critical period
The study suggests the following hypothesis: the small size of the hippocampus in patients with 22q11 deletion syndrome is defined in the mother 's uterus, probably because of. poor vascularity However, a "second shot" later in development could determine the continuation of the hippocampus atrophy and the onset of psychotic symptoms. The critical period of schizophrenia being adolescence, the team of Geneva is currently studying the possibility of preventing atrophy of the hippocampus to preserve its functions.
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