Schizophrenia, a severe mental illness, in which patients decipher reality strangely or let’s say abnormally. For them, the world is a cluster of confusing thoughts, images, and sounds. This brain disorder distorts the way a person thinks, acts, expresses emotions, perceives reality, and relates to others.
An estimated 0.5% of the general population is affected by the Schizophrenia. Previous studies have suggested that it takes a combination of genetic abnormalities of chromosome 22, called 22q11 deletion syndrome and environment to trigger the disease.
22q11 deletion syndrome is a neurogenetic disorder that targets chromosome 22. 30% of individuals influenced by the disorder end up developing psychotic symptoms explicit to schizophrenia, for example, sound-related fantasies, memory issues, an issue affecting their view of the real world, and troubles in social communications portrayed by strong paranoia.
However, not everyone who has the syndrome necessarily develops psychotic symptoms. Well, there’s much incorrect information out there about Schizophrenia as nobody knows the root cause.
Then, what causes the illness?
Scientists at the University of Geneva (UNIGE), Switzerland has shed light on it and offered the first answer after observing and analyzing several years of patients with deletion syndrome.
They found that the size of the hippocampus, the region of the brain responsible for memory and emotions, was smaller than normal yet followed the same developmental curve as in healthy subjects. However, when the first symptoms appear – for the most part in adolescence– the hippocampus atrophies significantly.
Stephan Eliez, a professor in the Department of Psychiatry in UNIGE’s Faculty of Medicine said, “It’s now known that schizophrenia is linked to the hippocampus, a complex area of the brain that carries out a vast amount of processes simultaneously linked to memory, imagination and the emotions.”
“Recent studies have shown that also people suffering from deletion syndrome have a smaller than average hippocampus. That’s why we studied the development of this structure in detail, so we could understand why some people affected by deletion syndrome eventually develop psychotic symptoms, while others don’t.”
Scientists have been following 275 patients aged 6 to 35 years for 18 years: a control groups of 135 individuals – i.e., individuals without genetic problems – and 140 people with deletion syndrome, including 53 with moderate to severe psychotic symptoms.
Each patient in the study group underwent an MRI every three years so that scientists could better determine their brain development. Scientists discovered that the hippocampus of the group affected by deletion syndrome, although smaller from the beginning, yet following the same growth curve to that of the control group.
Valentina Mancini, a researcher in UNIGE’s Department of Psychiatry, said, “This meant that we could hypothesize that the smaller size of the hippocampus originates in utero during its development in the womb.”
Eliez said, “We also observed the subfields of the hippocampus in detail, discovering that one of them – called CA3 – was not affected by the decrease in size. This subfield plays a crucial role in the work of memorization and seems stronger than the other subparts.”
Scientists then compared the developmental curves of the hippocampus in people with deletion syndrome but no psychotic symptoms with those who developed psychotic symptoms.
Mancini said, “There’s no doubt about our results: around the age of 17 or 18, people with schizophrenic symptoms experience drastic atrophy in the size of their hippocampus, and especially in the CA3 area, despite CA3 had initially managed to develop normally, unlike the other subfields.”
But Why?
However, scientists do not have any precise answer to explain the drastic drop in the development of this vital brain structure. In any case, their speculations are equipped towards natural elements, for example, stress or neuronal inflammation.
Mancini explained, “The hippocampus of individuals with deletion syndrome is smaller; this means it has to compensate for its size through hyperactivity. In the event of a huge stress factor, especially during the critical period of adolescence, this hyperactivity might lead to a significant rise in glutamate that ‘poisons’ the hippocampus and causes its atrophy. The psychotic symptoms may result from this hyper-compensation, which ends up destroying the hippocampus.”
The study suggests the following hypothesis: the small size of the hippocampus in patients with 22q11 deletion syndrome is defined in the mother’s womb, probably due to poor vascularisation. However, a “second hit” later in development might determine the further hippocampal atrophy and the emergence of psychotic symptoms. As the critical period for schizophrenia is adolescence, Geneva scientists are working on the possibility of preventing the atrophy of the hippocampus from preserving its functions.
The study is published in the journal Molecular Psychiatry.