## 5 Discussion
We know that occupational burnout only develops after prolonged stress, which again is associated with hippocampal dysfunction, and reduced P300 amplitude may be a result of changes in the hippocampus, in which chronic elevated HPA axis activity may be involved [59]. P300 is commonly associated with memory updating and attentional allocation [49,60]. Reduced P300 amplitude may also be seen as a contributing factor to or as objective physiological confirmation of attention and memory problems in patients with burnout [51]. It should be noted here that alpha power can be quantified in two ways: peak alpha frequency (PAF) and individual alpha frequency (IAF). The IAF is considered a more accurate measure of the spectral distribution than the PAF. IAF is assumed to be related to features of white matter structure, such as fiber density, axon diameter, and myelination, and reflects different neuronal processes other than alpha power [52]. PAF correlates negatively with subjective ratings of \"fatigue today\" and \"total fatigue\". PAF has been shown to be consistently associated with reduced cerebral blood flow and reduced cerebral oxygenation [61]. PAF has also been proposed as an indicator of \"cognitive readiness\" [62], as reduced PAF is associated with poorer performance on memory tasks [63]. Interestingly, the reported daytime fatigue and mild cognitive changes in patients with CSF may be explained by poor basal sleep drive [64]. Thus, classifying alpha power as a biomarker of burnout may be true as it is non-invasive, reliable, has trait-like characteristics, and is heritable. However, the specificity of alpha power, which is necessary to distinguish burnout from other disorders, is lacking. The P300 seems reasonable as a second indicator that can be added to diagnostic specificity and can help discriminate between psychopathologies. The goal of discovering and understanding the brain structures and neuronal networks relevant to burnout is related to the work construct. The discovery and understanding of the above mechanisms bring the prevention and treatment of burnout closer. Further research is needed to confirm the findings described above and help develop interventions and strategies to help those suffering from job burnout. This is of great scientific, clinical, social, and economic importance, as job burnout can significantly reduce the ability to perform work tasks [65]. Work-related fatigue is common among workers, such as those in car factories [66]. Serious illnesses (stroke, neuromuscular diseases) and injuries can affect job burnout and the ability to be employed and work, but knowledge of individual factors is limited [67,68]. Further diagnostic methods need to be linked to being an employee. The phenomenon of job burnout in remote working, which is becoming increasingly common during the COVID-19 pandemic period, also requires research. Previous research has focused on the relationships between stress, burnout, and biomarkers, while the review by [PERSON] et al. [69] summarized the immune and endocrine changes found in patients with burnout. The main interest in the literature seems to be the hypothalamic-pituitary-adrenal (HPA) axis, which can be disturbed by chronic stress and can be tested by measuring hormonal reactivity:  
* corticotropin-releasing hormone (CRH);
* adrenocortic hormone (ACTH);
* cortisol;
* prolactin;
* thyroid hormones;  
in the conditions of their pulsatile and diurnal fluctuation and heterogeneity of burnout measures [69; 70]. BDNF, the plasma level of which is higher in people with chronic stress, may play a key role in the mechanisms of stress-related disorders, and increasing its peripheral levels may contribute to the protection of neurons under stress [71].