Summary: The study reveals striking similarities in both behavior and neuroanatomical changes among people with schizophrenia and BMD.
source: Max Planck Institute
For the first time, researchers have compared schizophrenia and frontotemporal dementia, two disorders located in the frontal and temporal lobes of the brain.
The idea can be traced back to Emil Kraepelin, who coined the term “dementia praecox” in 1899 to describe the progressive mental and emotional deterioration of young patients. His method was soon challenged, with only 25% of sufferers showing this type of disease progression.
But now, with the help of imaging and machine learning, scientists have found the first valid indicators of neuroanatomical patterns in the brain that resemble the signature of patients with frontotemporal dementia.
It is rare for scientists in basic research to return results that seem outdated and are more than 120 years old. In the case of Nikolaos Koutsoliris and Matthias Schrotter, two researchers and two physicians, this served as a trigger.
It’s about Emil Kraepelin, founder of the Max Planck Institute of Psychiatry (MPI) as well as the Psychiatric Hospital of the Ludwig Maximilian University of Munich (LMU), and his term “early dementia”, coined in 1899.
This was his definition of young people increasingly withdrawing from reality and falling into an irreversible dementia-like state. Kraepelin lived to see his concept refuted.
By the beginning of the twentieth century, experts began to use the term “schizophrenia” for these patients, since the disease does not take a bad course in all the people involved.
Kraepelin had the idea of frontotemporal disease, and hypothesized that the cause of the sometimes debilitating course of patients lies in the frontal and temporal lobe regions of the brain. This is where personality, social behavior, and empathy are controlled.
“But this idea was lost because no pathological evidence for the neurodegenerative processes observed in Alzheimer’s disease was found in the brains of these patients,” says Koutsouleris, who works on the premises of Kraepelin, MPI and LMU.
He continues, “Since I became a psychiatrist, I’ve wanted to work on this question.” Fifteen years later, with large data sets, imaging techniques, and machine learning algorithms, the professor had the tools at hand to find potential answers.”
He has found the right partner in Matthias Schroeter, who studies neurodegenerative diseases, specifically frontotemporal dementia, at the Max Planck Institute for Human Cognitive and Brain Sciences.
Similarities Between Schizophrenia and Frontotemporal Dementia
Frontotemporal dementia (FTD), especially the behavioral variant (bvFTD), is difficult to recognize in its early stages because it is often confused with schizophrenia. Thus, the similarities are clear: in patients of both groups, personality as well as behavioral changes occur.
An often dramatic development for the affected people and their relatives. Since both disorders are located in the frontal, temporal, and insular regions of the brain, it was clear that they were also directly compared.
“They seem to be on the same spectrum of symptoms, so we wanted to look for common signatures or patterns in the brain,” says Koutsouleris, describing his plan.
With an international team, Koutsouleris and Schroeter used artificial intelligence to train neuroanatomical classifiers for both disorders, which they applied to brain data from different groups.
The result, just published in the magazine Gamma Psychiatrythat 41% of schizophrenia patients met the classifier criteria for bvFTD.
“When we saw this in schizophrenics as well, the bell rang — suggesting the similarity between the two disorders,” Coetsulliris and Schrötter recall.
The research team found that the higher the patients’ bvFTD score, which measures similarity between the two disorders, the more likely they were to have a “bvFTD-like” phenotype and the less likely their symptoms were to improve over a two-year period.
A 23-year-old patient is not recovering
“I just wanted to know why my 23-year-old patient who had symptoms of schizophrenia, such as hallucinations, delusions and cognitive deficits, didn’t improve at all, even after two years, while another equally bad patient was continuing his education and found a girlfriend. Time and time again, I saw these Young people who haven’t recovered at all,” Cozzoliris says.
When the researchers also examined associations in high-risk patients like the 23-year-old, they found neuroanatomical confirmation of what Kraepelin was first to conclusively describe: no improvement at all in some patients, absolutely. contrast.
Similar neural structures were affected, particularly the so-called default mode network and the brain’s salient network, which are responsible for controlling attention, empathy, and social behavior, and showed a reduction in volume in the gray matter area comprising neurons. In bvFTD, some neurons (von Economo neurons) die; In schizophrenia, these neurons also change. This was reflected in the neuroanatomical finding: after one year, it doubled in those severely affected people.
For comparison, scientists also calculated the Alzheimer’s disease score using a specific classifier and didn’t find these effects there.
“This means that the concept of emerging dementia can no longer be completely erased; we provide the first valid evidence that Kraepelin was not at fault, at least in some patients,” Schrotter says.
Today, or in the near future, this means that experts will be able to predict which subgroup patients belong to.
“Intensive therapeutic support can then be started at an early stage to exploit any remaining healing potential,” Cotsoliris says.
In addition, novel personalized therapies for this subgroup could be developed that promote proper maturation and connectivity of affected neurons and prevent their progressive destruction as part of the disease process.
About this research on schizophrenia and dementia news
author: press office
source: Max Planck Institute
Contact: Press Office – Max Planck Institute
picture: Photo credited to Koutsouléris
original search: Access closed.
“Exploring the Links Between Psychosis and Frontotemporal Dementia Using Multimodal Machine Learning” by Nikolaos Koutsoliris et al. Gamma Psychiatry
Exploring the links between psychosis and frontotemporal dementia using multimodal machine learning
The behavioral and cognitive symptoms of severe psychotic disorders overlap with those of dementia. However, joint brain changes remain in dispute, and their significance for patients in high-risk stages of the disease has not yet been explored.
to use machine learning to compare the expression of structural magnetic resonance imaging (MRI) patterns of behavioral variable frontotemporal dementia (bvFTD), Alzheimer’s disease (AD), and schizophrenia; Estimation of predictive power in patients with bvFTD and schizophrenia based on sociodemographic, clinical, and biological data; It examines the prognostic value, genetic underpinnings, and progression in patients with clinically high-risk (CHR) cases of psychosis or recent-onset depression (ROD).
Design, setup and participants
This study included 1,870 patients from 5 groups, including (1) patients with bvFTD (n = 108), AD (n = 44), mild cognitive impairment or early stage AD (n = 96), schizophrenia (n = 157), or major depressive (n = 102) to derive and compare diagnostic patterns and (ii) patients with CHR (n = 160) or ROD (n = 161) to test the relevance and evolution of patterns. Healthy individuals (n = 1042) were used to calibrate the data related to age and cohort. Data was collected from January 1996 to July 2019 and analyzed between April 2020 and April 2022.
Main findings and measures
Case assignments based on diagnostic patterns; sociodemographic, clinical and biological data; 2-year functional outcome and genetic segregation of patients with CHR and ROD with high versus low phenotype expression; The pattern progressed from baseline to follow-up MRI scans in patients with no recovery versus preserved recovery.
Of the 1870 patients included, 902 (48.2%) were female, and the mean age (SD) was 38.0 (19.3) years. The bvFTD pattern comprising reductions in frontal, insular, and limbic lobe volumes was more highly expressed in patients with schizophrenia (65 out of 157). [41.2%]) and major depression (22 out of 102 .) [21.6%]) of AD patterns the limbic rhythm (28 of 157 [17.8%] and 3 of 102 [2.9%], Straight). bvFTD expression was predicted by elevated body mass index, psychomotor slowing, emotional purging, and paranoid thinking (s2= 0.11). The schizophrenia pattern was expressed in 92 of 108 patients (85.5%) with bvFTD and was associated with C9orf72 Variable, oligoclonal banding in CSF, cognitive impairment, and younger age (s2= 0.29). bvFTD and schizophrenia pattern expressions predicted 2-year psychosocial impairment in patients with CHR and were predicted by polygenic risk scores for frontotemporal dementia, Alzheimer’s disease, and schizophrenia. The results were not related to Alzheimer’s disease or accelerated brain aging. Finally, the 1-year bvFTD/schizophrenia pattern progression distinguished patients with no recovery from those with preserved recovery.
Conclusions and relevance
Neurobiological links may exist between bvFTD and psychosis with a focus on alterations of the prefrontal and paraventricular system. Further cross-diagnostic investigations are needed to identify the common pathophysiological processes underlying the neuroanatomical interface between the 2 disease spectra.
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