Prof Amy Milton

Mitochondrial dysfunction in PTSD: A mechanism to understand trauma susceptibility? - Psychopharmacology Rationale and Objectives Post-Traumatic Stress Disorder (PTSD) is a complex mental health condition that arises following exposure to traumatic events. Converging evidence suggests mitochondrial dysfunction and brain energy metabolism impairment in its pathophysiology. Thus, examining mitochondrial data from both preclinical and experimental medicine studies may help us to have a deeper understanding of the pathophysiological mechanisms underlying PTSD. Methods Using PubMed, Scopus and Web of Science online databases, we conducted a search for peer-reviewed manuscripts targeting both mitochondrial-related activity and PTSD. Our search yielded 43 studies in total, including 29 in rodent models and 15 clinical studies. Results Preclinical studies reported a decrease in energy metabolism with a reduction in adenosine triphosphate (ATP) level, upregulation of genes associated with ATP synthesis, impairment of the glycolytic pathway, citric acid cycle and oxidative phosphorylation pathways and increased oxidative stress and neuronal apoptosis in the brain, or systemically. In the clinical setting, studies identified 1108 participants with PTSD and 312 with partial PTSD, with these individuals showing alterations in energy production, mitochondrial DNA copy number (mtDNAcn) and elevated oxidative stress. Risperidone and AC-5216—a selective ligand for TSPO—emerged as potential treatments. Conclusion Our synthesis of the published findings indicates a notable overlap between results from both animal models and humans which could show a potential usage of mitochondrial-related targets as biomarkers or for drug discovery. Additionally, these results highlight the need for future research in describing whether mitochondrial dysfunction is a cause or a symptom of PTSD.

Great to see Felippe Espinelli Amorim’s (not yet on BlueSky) and @charlotte-rye.bsky.social’s meta-analysis on mitochondrial dysfunction in PTSD out in @psychopharmacology.bsky.social 👏🏻
link.springer.com/article/10.1...

Reward contamination in restrictive anorexia nervosa: A meta-analysis of functional MRI studies Individuals with anorexia nervosa (AN) are typically anhedonic, leading to the suggestion that intrinsic disturbances of reward processing may represe…

I'm excited to share that our meta-analysis on reward-related brain activity in anorexia nervosa has been published in Pharmacology, Biochemistry and Behavior!

Thanks to @profamymilton.bsky.social @camneuro.bsky.social for helping bring this to life!

www.sciencedirect.com/science/arti...

Agonism at mGluR2 receptors reduces dysfunctional checking on a rodent analogue of compulsive-like checking in obsessive compulsive disorder - Psychopharmacology Rationale Obsessive-compulsive disorder (OCD) affects 1–3% of the population. Current therapies, including selective serotonin reuptake inhibitors, are not universally effective in managing OCD. Recen...

🚨 Another new paper alert 🚨
This one on our finding that drugs targeting mGluR2 rapidly reduce checking in a rodent model relevant to OCD.

link.springer.com/article/10.1...

Glutamate receptor expression in the PL-BLA circuit is associated with susceptibility to showing the PTSD-like phenotype While many individuals experience traumatic events during their lifetimes, only some go on to develop post-traumatic stress disorder (PTSD). This susc…

🚨 New paper alert 🚨
Very proud to share Charlotte Rye’s paper from her MPhil work. (She’s not yet on BlueSky but I’ll work on that.) Thank you to @camneuro.bsky.social for all the support 🙏🏻

www.sciencedirect.com/science/arti...