In Search of Neurobiological Factors for Schizophrenia

Summary: Researchers find no appreciable differences between the hippocampi of those at high risk for developing schizophrenia and those with the disorder.

Source: University of Basel.

Schizophrenic psychoses are a frequently occurring group of psychiatric disorders caused by a combination of biological, social and environmental factors. These disorders are associated with changes to the brain structure: for example, the hippocampus in the temporal lobe is usually smaller in affected individuals than in healthy ones. It is not yet known whether these changes to the brain structure are a result of the disorders and their accompanying medications, or whether they are already present before the onset of symptoms.

Together with a research group from the University of Basel, Fabienne Harrisberger and Stefan Borgwardt examined the brain structures of individuals exhibiting an elevated risk of psychosis, and those of individuals experiencing the onset of psychotic symptoms for the first time. Initially, scientists from the Adult Psychiatric Clinic of the University Psychiatric Clinics (UPK) and the Transfaculty Research Platform Molecular and Cognitive Neurosciences (MCN) observed no appreciable difference between the hippocampi of individuals at high risk and those of patients.

Next, together with scientists from the Transfaculty Research Platform, they investigated whether any known schizophrenia risk genes are associated with the hippocampus. This appears to be the case: the greater the number of risk genes a person possessed, the smaller the volume of their hippocampus – regardless of whether they were a high-risk study participant or a patient. This means that a group of risk genes is connected with a reduction in the size of a critical region of the brain before the disorder manifests itself.

Potential for differentiated therapy

This result is significant for the understanding of neurobiological factors contributing to schizophrenia. It is well-known that none of the wider risk factors (e.g. genes, environment, unfavorable social situation) can be used to predict the onset of psychosis in a specific individual. However, the discovery may be of use for the treatment of schizophrenia.

Image shows the location of the hippocampus in the human brain.
This image shows the location of the hippocampus in the human brain: sagittal and axial view (from left to right) of the hippocampus (yellow) in an MRI. NeuroscienceNews.com image is credited to Neuropsychiarty and Brain Imaging Group, Basel.

“It is quite possible that individuals with smaller hippocampi will react differently to therapy compared to those with normally developed hippocampi,” explains Prof. Stefan Borgwardt of the Neuropsychiatry and Brain Imaging Unit. Further studies to ascertain the therapeutic potential of this research are planned.

About this psychology research article

Source: Olivia Poisson – University of Basel
Image Source: This NeuroscienceNews.com image is credited to Neuropsychiarty and Brain Imaging Group, Basel.
Original Research: Full open access research for “Impact of polygenic schizophrenia-related risk and hippocampal volumes on the onset of psychosis” by F Harrisberger, R Smieskova, C Vogler, T Egli, A Schmidt, C Lenz, A E Simon, A Riecher-Rössler, A Papassotiropoulos and S Borgwardt in Translational Psychiatry. Published online August 9 2016 doi:10.1038/tp.2016.143

Cite This NeuroscienceNews.com Article

[cbtabs][cbtab title=”MLA”]University of Basel. “In Search of Neurobiological Factors for Schizophrenia.” NeuroscienceNews. NeuroscienceNews, 9 August 2016.
<https://neurosciencenews.com/schizophrenia-neurobiology-4808/>.[/cbtab][cbtab title=”APA”]University of Basel. (2016, August 9). In Search of Neurobiological Factors for Schizophrenia. NeuroscienceNew. Retrieved August 9, 2016 from https://neurosciencenews.com/schizophrenia-neurobiology-4808/[/cbtab][cbtab title=”Chicago”]University of Basel. “In Search of Neurobiological Factors for Schizophrenia.” https://neurosciencenews.com/schizophrenia-neurobiology-4808/ (accessed August 9, 2016).[/cbtab][/cbtabs]


Abstract

Impact of polygenic schizophrenia-related risk and hippocampal volumes on the onset of psychosis

Alterations in hippocampal volume are a known marker for first-episode psychosis (FEP) as well as for the clinical high-risk state. The Polygenic Schizophrenia-related Risk Score (PSRS), derived from a large case–control study, indicates the polygenic predisposition for schizophrenia in our clinical sample. A total of 65 at-risk mental state (ARMS) and FEP patients underwent structural magnetic resonance imaging. We used automatic segmentation of hippocampal volumes using the FSL-FIRST software and an odds-ratio-weighted PSRS based on the publicly available top single-nucleotide polymorphisms from the Psychiatric Genomics Consortium genome-wide association study (GWAS). We observed a negative association between the PSRS and hippocampal volumes (β=−0.42, P=0.01, 95% confidence interval (CI)=(−0.72 to −0.12)) across FEP and ARMS patients. Moreover, a higher PSRS was significantly associated with a higher probability of an individual being assigned to the FEP group relative to the ARMS group (β=0.64, P=0.03, 95% CI=(0.08–1.29)). These findings provide evidence that a subset of schizophrenia risk variants is negatively associated with hippocampal volumes, and higher values of this PSRS are significantly associated with FEP compared with the ARMS. This implies that FEP patients have a higher genetic risk for schizophrenia than the total cohort of ARMS patients. The identification of associations between genetic risk variants and structural brain alterations will increase our understanding of the neurobiology underlying the transition to psychosis.

“Impact of polygenic schizophrenia-related risk and hippocampal volumes on the onset of psychosis” by F Harrisberger, R Smieskova, C Vogler, T Egli, A Schmidt, C Lenz, A E Simon, A Riecher-Rössler, A Papassotiropoulos and S Borgwardt in Translational Psychiatry. Published online August 9 2016 doi:10.1038/tp.2016.143

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