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Stress is a ubiquitous challenge in modern societies. Symptoms range from mood swings and cognitive impairment to autonomic symptoms. This study explores the link between work-related stress and the neurobiological element of brain processing, testing the hypothesis that patients with occupational stress have altered cerebral glucose consumption compared to healthy controls. The participants' present conditions were evaluated using an adapted WHO SCAN interview. Neural activity at rest was assessed by positron emission tomography (PET) with the glucose analogue [18F]fluorodeoxyglucose. Participants were genotyped for the Val158Met polymorphism of the COMT gene, believed to influence stress resilience. This study included 11 women with work-related stress and 11 demographically comparable healthy controls aged 28–62 years, with an average of 46.2 years. The PET scans indicated clusters of decreased glucose consumption primarily located in the white matter of frontal lobe sub-gyral areas in stress patients. COMT Val158Met polymorphism detection indicated no immediate relation of the homozygous alleles and stress resilience; however, healthy controls mainly had the heterozygous allele. In conclusion, the results support that work-related stress does affect the brain in the form of altered glucose metabolism, suggesting neurobiological effects could be related to white matter abnormalities rather than gray matter deterioration. Genotyping indicates a more complex picture than just that of the one type being more resilient to stress. Further studies recruiting a larger number of participants are needed to confirm our preliminary findings. [ABSTRACT FROM AUTHOR]

Introduction: Stress is one of the greatest burdens of our society and often implies impairments in cognitive and emotional functions. Here, we hypothesise that changes in the brain's dopamine (DA)-based mesocorticolimbic projec-tions in patients with work-related stress (adjustment disorder) will manifest themselves as altered glucose metabolism in relation to neural activity, and as altered DA radiotracer binding potentials at the relevant receptors., Methods: Subjects and healthy controls undergo neuropsychiatric tests and PET/MRI with three tracers: 18F-fluorodeoxyglucose to measure glucose metabolism as a marker of neural activity, 11C-raclopride to explore binding potentials in the striatum, and 11C-FLB 457 to study possibly impaired mesocortical dopaminergic transmission in the cortex. To demonstrate differences of glucose metabolism, more than 2 × 41 patients/controls are needed. We expect to find that symptoms of cognitive and motivational reward deficits are attributable to changes in the frontal lobe and striatal glucose metabolism in the majority of patients, and that changes of D2-receptor availability and impaired dopaminergic transmission in the striatum and prefrontal cortex are contributing factors., Conclusions: This project is designed to generate entirely new and objective evidence of stress-induced cerebral illness, and to provide a basis for in-depth research and for a more rational management of this strenuous disorder., Funding: Private, industrial and public funds., Trial Registration: Clinicaltrails.gov/NCT03334045., (Articles published in the DMJ are “open access”. This means that the articles are distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits any non-commercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.)