Hippocampal–prefrontal connectivity as a translational phenotype for schizophrenia

Bähner, Florian; Meyer‐Lindenberg, Andreas

doi:10.1016/j.euroneuro.2016.12.007

Cited by 73 publications

(52 citation statements)

References 138 publications

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“…In this study, it was found that the white matter ber in the right hippocampal region was more seriously damaged in DS patients, and it was signi cantly correlated with duration of education , duration of antipsychotic use, and the PANSSnegative symptoms score. This supports the conclusions of some previous studies, providing a possible explanation for the more severe cognitive impairment seen in DS patients [15] .…”

Section: Resultssupporting

confidence: 92%

A Study of the Characteristics of the White Matter in Schizophrenic Patients with Defective or Non-defective Symptoms by Diffuse Tensor Imaging

Shi¹,

Sun²,

Zhuang³

et al. 2020

Preprint

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BackgroundDeficit schizophrenia (DS) is a set of highly homogenous schizophrenia subtypes characterized by primary and persistent negative symptoms. Previous research studies have found that the negative symptoms of schizophrenia are closely related to the impairment of brain structure and function.This study seeks to explore the characteristics of white matter in schizophrenic patients with defective or non-defective symptoms by diffuse tensor imaging (DTI).MethodsAccording to the defective schizophrenia diagnostic criteria and ICD-10 diagnostic criteria, 30 patients with DS and 30 patients with non-defective schizophrenia (NDS) were enrolled into the research study. DTI imaging data of the white matter were collected by 1.5T magnetic resonance imaging scanner. Then a tract-based spatial statistics (TBSS) method was used to compare the fractional anisotropy (FA) values of the white matter fiber between the two groups.ResultsThe TBSS analysis results showed that the FA values in the right side of the knee of the corpus callosum (MNI:14,36,-7), right anterior radio-coronal region (MIN:11,34,3) and the right hippocampal region (MIN:30,34,16) in the DS patients were significantly lower compared with those of the NDS patients (all p<0.05). The FA values in the right side of the knee of the corpus callosum was significantly correlated with the time from onset to treatment (r=−0.350, p<0.001), PANSS-negative symptom score (r=−0.157, p=0.007). The FA values in the right anterior radio-crown region was positively correlated with PANSS-negative symptom score (r=0.306, p=0.048). The right hippocampus was negatively correlated with years of education (r=−0.614, p=0.020), duration of antipsychotics using(r=−0.140, p= 0.022), and PANSS-negative symptom score (r=−0.637, p=0.040).ConclusionsIn schizophrenic patients with defective symptoms, the structural integrity of white matter fibers was more seriously damaged in the three brain regions including the right knee of the corpus callosum, the right anterior region of the right radiative crown, and the right hippocampus. These white matter lesions are closely related to patient characteristics such as years of education, duration from onset to treatment, duration of anti-psychotic, and severity of negative symptoms.

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Section: Resultssupporting

confidence: 92%

A Study of the Characteristics of the White Matter in Schizophrenic Patients with Defective or Non-defective Symptoms by Diffuse Tensor Imaging

Shi¹,

Sun²,

Zhuang³

et al. 2020

Preprint

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“…Indeed, in healthy controls performing high working memory load tasks, the HPC deactivates and functionally uncouples from the dlPFC. Such an anticorrelated pattern is, however, disrupted in chronic and first‐episode patients with schizophrenia and individuals at high‐risk of psychosis . This observation has been replicated in several studies using different methodologies.…”

Section: Discoordination In Large‐scale Networkmentioning

confidence: 66%

Neural and neuronal discoordination in schizophrenia: From ensembles through networks to symptoms

et al. 2019

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Despite the substantial knowledge accumulated by past research, the exact mechanisms of the pathogenesis of schizophrenia and causal treatments still remain unclear. Deficits of cognition and information processing in schizophrenia are today often viewed as the primary and core symptoms of this devastating disorder. These deficits likely result from disruptions in the coordination of neuronal and neural activity. The aim of this review is to bring together convergent evidence of discoordinated brain circuits in schizophrenia at multiple levels of resolution, ranging from principal cells and interneurons, neuronal ensembles and local circuits, to large-scale brain networks. We show how these aberrations could underlie deficits in cognitive control and other higher order cognitive-behavioural functions. Converging evidence from both animal models and patients with schizophrenia is presented in an effort to gain insight into common features of deficits in the brain information processing in this disorder, marked by disruption of several neurotransmitter and signalling systems and severe behavioural outcomes. K E Y W O R D SfMRI, GABA interneurons, humans, oscillations, psychosis, rats

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“…All of this information gives an important framework for meaningful interpretation of the proteomic data. Given the documented role of hippocampal pathology in cognitive impairment in SZ [49][50][51][52] it would be logical to hypothesize that these gross changes play a critical part in the development of SZ-related endophenotypes in the Fgf14-/-mice. An additional advantage is that hippocampus can be readily isolated from the adjacent brain structures, which makes sample preparation more robust and reproducible.…”

Section: Resultsmentioning

confidence: 99%

Sex-Specific Proteomics Changes Induced by Genetic Deletion of the Fibroblast Growth Factor 14 (FGF14) Regulator of Neuronal Ion Channels

Sowers¹,

Re²,

Wadsworth³

et al. 2018

Preprint

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Fibroblast growth factor 14 (FGF14) is a member of the intracellular FGFs, a group of proteins with roles in neuronal ion channel regulation and synaptic transmission. We have previously demonstrated that a male Fgf14-/- mouse model recapitulates salient endophenotypes of synaptic dysfunction and behaviors associated with schizophrenia (SZ). As the underlying etiology of SZ and its sex-specific onset remain elusive, the Fgf14-/- model provides a valuable tool to interrogate pathways that might be related to the disease mechanism. Here, we performed label free quantitative proteomics and bioinformatics to identify enriched pathways at the proteome level in the male and female hippocampi from Fgf14+/+ and Fgf14-/- mice. We discovered that many differentially expressed proteins in Fgf14-/- animals are associated with SZ. In addition, measured changes in the proteome and signaling pathways were predominantly sex-specific with the male Fgf14-/- being distinctly enriched for pathways associated with neuropsychiatric disorders and addiction and the female exhibiting modest changes. In the male Fgf14-/- mouse the major protein changes that could in part explain the previously described neurotransmission and behavioral phenotype of this model were loss of ALDH1A1 and PRKAR2B. ALDH1A1 has been shown to mediate an alternative pathway for GABA synthesis, while PRKAR2B is essential for dopamine 2 receptor signaling, which is the basis of current antipsychotics. Collectively, our results provide new insights in the role of FGF14 and support the use of the Fgf14-/- mouse as a useful preclinical model of SZ for generating hypothesis on the disease mechanism, sex-specific manifestation and therapy.

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Hippocampal–prefrontal connectivity as a translational phenotype for schizophrenia

Cited by 73 publications

References 138 publications

A Study of the Characteristics of the White Matter in Schizophrenic Patients with Defective or Non-defective Symptoms by Diffuse Tensor Imaging

A Study of the Characteristics of the White Matter in Schizophrenic Patients with Defective or Non-defective Symptoms by Diffuse Tensor Imaging

Neural and neuronal discoordination in schizophrenia: From ensembles through networks to symptoms

Sex-Specific Proteomics Changes Induced by Genetic Deletion of the Fibroblast Growth Factor 14 (FGF14) Regulator of Neuronal Ion Channels

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