ArticleSchizophrenia research2018
Translocator protein (TSPO) and stress cascades in mouse models of psychosis with inflammatory disturbances.
Article in Schizophrenia research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Maternal immune activation followed by peripubertal stress combinedly produce reactive microglia and confine cerebellar cognition.Communications biology · 2025Article
- The protective effect of PK11195 on D-galactose-induced amnestic mild cognitive impairment in rats.Annals of translational medicine · 2020Article
- Selective, high-contrast detection of syngeneic glioblastoma in vivo.Scientific reports · 2020Article
- Personality traits in psychosis and psychosis risk linked to TSPO expression: a neuroimmune marker.Personality neuroscience · 2020Article
- Expression of Translocator Protein and [18F]-GE180 Ligand Uptake in Multiple Sclerosis Animal Models.Cells · 2019Article
- Molecular Imaging of Immune Cell Dynamics During De- and Remyelination in the Cuprizone Model of Multiple Sclerosis by [Theranostics · 2019Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Changes in inflammatory cascades have been implicated in the underlying pathophysiology of psychosis. Translocator protein 18 kDa (TSPO) has been used to assess neuroinflammatory processes in psychotic disorders. Nonetheless, it is unclear whether TSPO, a mitochondrial protein, can be interpreted as a general marker for inflammation in diseases involving psychosis. To address this question, we investigated TSPO signaling in representative mouse models for psychosis with inflammatory disturbances. The maternal immune activation and cuprizone short-term exposure models show different TSPO signaling. Furthermore, we observed similarities and differences in their respective stress pathways including stress hormone signaling and oxidative stress that are functionally interconnected with the inflammatory responses. We propose that more careful studies of TSPO distribution in neuroinflammation and other stress cascades associated with psychotic symptoms will allow us to understand the biological mechanisms underlying psychosis-related behaviors.
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Registered trials
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