Myelination and oxidative stress alterations in the cerebellum of the G72/G30 transgenic schizophrenia mouse model
Abstract
G72/G30 is a primate-specific locus that has been repeatedly implicated as a risk factor in genetic studies of schizophrenia. The function of the longest G72 splice variant (LG72 protein) encoded by this locus is not fully understood. To investigate the role of the LG72 protein in vivo, we have generated transgenic (G72Tg) mice carrying the G72/G30 locus that exhibit schizophrenia-like symptoms. We investigated protein expression alterations in the cerebella of G72Tg compared to wild type (WT) mice using a proteomics approach based on in vivo(15)N metabolic labeling and quantitative mass spectrometry (MS). Our data revealed expression level differences of proteins involved in myelin-related processes, oxidative stress and mitochondrial function. Furthermore, in silico pathway analyses suggested common regulators and targets for the observed protein alterations. Our work sheds light on the functional role of the LG72 protein and pinpoints molecular correlates of schizophrenia-like behavior.
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NAC treatment prevents PVI abnormalities in the NVHL model and blocking superoxide overproduction by NADPH oxidase prevents the PVI impairment induced by social isolation.
“Evidence causally linking oxidative stress to PVI deficits in other schizophrenia models also exists: NAC treatment prevents PVI abnormalities in the NVHL model 56 and blocking superoxide overproduction by NADPH oxidase (NOX) prevents the PVI impairment induced by social isolation 64 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [56]
Juvenile antioxidant treatment using N-acetyl cysteine prevents oxidative stress in a developmental rat model of schizophrenia (neonatal ventral hippocampal lesion) and inhibits the emergence of morphological, electrophysiological and behavioural deficits.
“The causal relevance of oxidative stress was further strengthened by the demonstration that juvenile antioxidant treatment using N-Acetyl cysteine (NAC) prevents oxidative stress in a developmental rat model of schizophrenia (neonatal ventral hippocampal lesion (NVHL)) and, in doing so, inhibits the emergence of morphological, electrophysiological and behavioural deficits 56 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [56]
The potential for juvenile NAC treatment to prevent the emergence of electrophysiological and behavioural deficits in a rodent developmental model of schizophrenia suggests that prophylactic treatment for high-risk groups may be effective.
“The potential for juvenile NAC treatment to prevent the emergence of electrophysiological and behavioural deficits in a rodent developmental model of schizophrenia 56 suggests that prophylactic treatment for high-risk groups may be effective, particularly with a drug or dietary supplement with a good safety profile like NAC or polyunsaturated fatty acids such as omega 3s 105 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [56]
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- Authors
- Filiou, M. D., Teplytska, L., Otte, D. M., Zimmer, A., & Turck, C. W.
- Affiliations
- Max Planck Institute of Psychiatry (DE)
- Max Planck Society (DE)
- University of Bonn (DE)
- Corresponding author
- Filiou, Michaela D.
- Venue
- Journal of Psychiatric Research
- Publisher
- Elsevier BV
- Published
- 2012-10
- Volume
- 46
- Issue
- 10
- Pages
- 1359-1365
- ISSN
- 0022-3956 (ISSN-L)
- OpenAlex
- W2079772279
- Cited by
- 36
- References
- 48
- Citations by year
- 2025: 2 · 2024: 2 · 2022: 4 · 2021: 1 · 2020: 2 · 2019: 3 · 2017: 2 · 2016: 6 · 2015: 4 · 2014: 5 · 2013: 4 · 2012: 1
- FWCI
- 3.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Psychiatric Research (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- schizophrenia, transgenic mouse model, cerebellum, myelination, oxidative stress, mitochondrial function, proteomics, schizophrenia risk genes
- MeSH terms
- Animals, Carrier Proteins, Catalase, Cerebellum, Disease Models, Animal, Female, Gene Expression Regulation, Humans, Male, Mice, Transgenic, Mutation, Nerve Fibers, Myelinated, Nitrogen Isotopes, Schizophrenia, Mass Spectrometry, Reproducibility of Results, Oxidative Stress, Genetic Predisposition to Disease, Proteomics, Intracellular Signaling Peptides and Proteins, Mice
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