No association between the protein tyrosine phosphatase, receptor‐type, Z Polypeptide 1 (<i>PTPRZ1</i>) gene and schizophrenia in the Japanese population

Ito, Yoshihito; Yamada, Shinnosuke; Takahashi, Nagahide; Saito, Shinichi; Yoshimi, Akira; Inada, Toshiya; Noda, Yukihiro; Ozaki, Norio

doi:10.1002/ajmg.b.30692

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…RPTPβ is expressed in oligodendrocytes, and appears to modulate ERBB4 signaling. Association analysis of PTPRZ1 showed highly significant association of this gene to schizophrenia in this first study, however, this association was not replicated in a Japanese cohort (Ito et al, 2008). …”

Section: Geneticsmentioning

confidence: 58%

Linking white and grey matter in schizophrenia: Oligodendrocyte and neuron pathology in the prefrontal cortex

et al. 2009

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Neuronal circuitry relies to a large extent on the presence of functional myelin produced in the brain by oligodendrocytes. Schizophrenia has been proposed to arise partly from altered brain connectivity. Brain imaging and neuropathologic studies have revealed changes in white matter and reduction in myelin content in patients with schizophrenia. In particular, alterations in the directionality and alignment of axons have been documented in schizophrenia. Moreover, the expression levels of several myelin-related genes are decreased in postmortem brains obtained from patients with schizophrenia. These findings have led to the formulation of the oligodendrocyte/myelin dysfunction hypothesis of schizophrenia. In this review, we present a brief overview of the neuropathologic findings obtained on white matter and oligodendrocyte status observed in schizophrenia patients, and relate these changes to the processes of brain maturation and myelination. We also review recent data on oligodendrocyte/myelin genes, and present some recent mouse models of myelin deficiencies. The use of transgenic and mutant animal models offers a unique opportunity to analyze oligodendrocyte and neuronal changes that may have a clinical impact. Lastly, we present some recent morphological findings supporting possible causal involvement of white and grey matter abnormalities, in the aim of determining the morphologic characteristics of the circuits whose alteration leads to the cortical dysfunction that possibly underlies the pathogenesis of schizophrenia.

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Section: Geneticsmentioning

confidence: 58%

Linking white and grey matter in schizophrenia: Oligodendrocyte and neuron pathology in the prefrontal cortex

et al. 2009

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“…Recent studies suggested that proteoglycans regulate Neuregulin/ErbB signaling, and thus are related to psychiatric disorders. Buxbaum et al ( 2008 ) reported that PTPRZ1 , which encodes both PTPζ and phosphacan, is associated with schizophrenia in a Caucasian population, although no association was found in the Japanese population (Ito et al, 2008 ). They demonstrated that PTPζ binds with ErbB4 through the scaffolding protein, MAGI, and inhibits the Neuregulin-1/ErbB4 signaling.…”

Section: Proteoglycans Psychiatric Disorders and Intellectual Disabmentioning

confidence: 99%

Proteoglycans and neuronal migration in the cerebral cortex during development and disease

2015

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Chondroitin sulfate proteoglycans and heparan sulfate proteoglycans are major constituents of the extracellular matrix and the cell surface in the brain. Proteoglycans bind with many proteins including growth factors, chemokines, axon guidance molecules, and cell adhesion molecules through both the glycosaminoglycan and the core protein portions. The functions of proteoglycans are flexibly regulated due to the structural variability of glycosaminoglycans, which are generated by multiple glycosaminoglycan synthesis and modifying enzymes. Neuronal cell surface proteoglycans such as PTPζ, neuroglycan C and syndecan-3 function as direct receptors for heparin-binding growth factors that induce neuronal migration. The lectican family, secreted chondroitin sulfate proteoglycans, forms large aggregates with hyaluronic acid and tenascins, in which many signaling molecules and enzymes including matrix proteases are preserved. In the developing cerebrum, secreted chondroitin sulfate proteoglycans such as neurocan, versican and phosphacan are richly expressed in the areas that are strategically important for neuronal migration such as the striatum, marginal zone, subplate and subventricular zone in the neocortex. These proteoglycans may anchor various attractive and/or repulsive cues, regulating the migration routes of inhibitory neurons. Recent studies demonstrated that the genes encoding proteoglycan core proteins and glycosaminoglycan synthesis and modifying enzymes are associated with various psychiatric and intellectual disorders, which may be related to the defects of neuronal migration.

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“…FGD4 is widely involved in the myelination of the vertebrate nervous system, and its deficiency can trigger the demyelination of the peripheral nerves in patients [ 47 , 48 ]. As a protein tyrosine phosphatase, PTPRZ1 is seen as a potential susceptibility gene for schizophrenia [ 49 , 50 , 51 ]. Study reports suggest that NEBL is associated with small and medium-sized vasculitis in Kawasaki disease, which, combined with GO analysis, suggests a possible association with neuronal projection and recognition [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Cortex Single-Cell Transcriptome and Serum Proteome Reveals the Novel Biomarkers in Alzheimer’s Disease

Feng

Shi

et al. 2022

Brain Sciences

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Blood-based proteomic analysis is a routine practice for detecting the biomarkers of human disease. The results obtained from blood alone cannot fully reflect the alterations of nerve cells, including neurons and glia cells, in Alzheimer’s disease (AD) brains. Therefore, the present study aimed to investigate novel potential AD biomarker candidates, through an integrated multi-omics approach in AD. We propose a comprehensive strategy to identify high-confidence candidate biomarkers by integrating multi-omics data from AD, including single-nuclei RNA sequencing (snRNA-seq) datasets of the prefrontal and entorhinal cortices, as wells as serum proteomic datasets. We first quantified a total of 124,658 nuclei, 8 cell types, and 3701 differentially expressed genes (DEGs) from snRNA-seq dataset of 30 human cortices, as well as 1291 differentially expressed proteins (DEPs) from serum proteomic dataset of 11 individuals. Then, ten DEGs/DEPs (NEBL, CHSY3, STMN2, MARCKS, VIM, FGD4, EPB41L2, PLEKHG1, PTPRZ1, and PPP1R14A) were identified by integration analysis of snRNA-seq and proteomics data. Finally, four novel candidate biomarkers (NEBL, EPB41L2, FGD4, and MARCKS) for AD further stood out, according to bioinformatics analysis, and they were verified by enzyme-linked immunosorbent assay (ELISA) verification. These candidate biomarkers are related to the regulation process of the actin cytoskeleton, which is involved in the regulation of synaptic loss in the AD brain tissue. Collectively, this study identified novel cell type-related biomarkers for AD by integrating multi-omics datasets from brains and serum. Our findings provided new targets for the clinical treatment and prognosis of AD.

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No association between the protein tyrosine phosphatase, receptor‐type, Z Polypeptide 1 (PTPRZ1) gene and schizophrenia in the Japanese population

Cited by 4 publications

References 36 publications

Linking white and grey matter in schizophrenia: Oligodendrocyte and neuron pathology in the prefrontal cortex

Linking white and grey matter in schizophrenia: Oligodendrocyte and neuron pathology in the prefrontal cortex

Proteoglycans and neuronal migration in the cerebral cortex during development and disease

Integrated Analysis of Cortex Single-Cell Transcriptome and Serum Proteome Reveals the Novel Biomarkers in Alzheimer’s Disease

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