ArticleBrain, behavior, & immunity - health2020
Cerebellar mitochondrial dysfunction and concomitant multi-system fatty acid oxidation defects are sufficient to discriminate PTSD-like and resilient male mice.
Article in Brain, behavior, & immunity - health, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Mitochondrial dysfunction in PTSD: A mechanism to understand trauma susceptibility?Psychopharmacology · 2026Review
- Recent advances in the role of miRNAs in post-traumatic stress disorder and traumatic brain injury.Molecular psychiatry · 2023Review
- The associations between metabolic profiles and sexual and physical abuse in depressed adolescent psychiatric outpatients: an exploratory pilot study.European journal of psychotraumatology · 2023Article
- Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD).Frontiers in physiology · 2023Review
- Outcomes of mitochondrial long chain fatty acid oxidation and carnitine defects from a single center metabolic genetics clinic.Orphanet journal of rare diseases · 2022Review
- Review
- Cerebellar and multi-system metabolic reprogramming associated with trauma exposure and post-traumatic stress disorder (PTSD)-like behavior in mice.Neurobiology of stress · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impact of trauma on mental health is complex with poorly understood underlying mechanisms. Mitochondrial dysfunction is increasingly implicated in psychopathologies and mood disorders, including post-traumatic stress disorder (PTSD). We hypothesized that defects in mitochondrial energy metabolism in the cerebellum, an emerging region of interest in the pathobiology of mood disorders, would be associated with PTSD-like symptomatology, and that PTSD-like symptomatology would correlate with the activities of the mitochondrial electron transport chain (mtETC) and fatty acid oxidation (FAO) pathways. We assayed mitochondrial energy metabolism and fatty acid profiling using targeted metabolomics in mice exposed to a recently developed paradigm for PTSD-induction. 48 wild type male FVB.129P2 mice were exposed to a trauma, and PTSD-like and resilient animals were identified using behavioral profiling. Mice displaying PTSD-like symptomatology displayed reduced mtETC complex activities in the cerebellum, and cerebellar mtETC complex activity negatively correlated with PTSD-like symptomatology. PTSD-like animals also displayed fatty acid profiles consistent with FAO dysfunction in both cerebellum and plasma. Machine learning analysis of all biochemical measures in this cohort of animals also identified plasma acetylcarnitine, along with reduced activity of cerebellar complex I and IV as well as succinate:cytochrome c oxidoreductase as state predictive discriminators of PTSD-symptomatology. Our data also suggest that trauma-induced impaired mtETC function in the cerebellum and concomitant impaired multi-system fatty acid oxidation are candidate drivers of PTSD-like behavior in mice. These bioenergetic and metabolic changes may offer an informative window into the underlying biology and highlight novel potential targets for diagnostics and therapeutic interventions in PTSD.
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