Nejvíce citovaný článek - PubMed ID 22023357
BACKGROUND/OBJECTIVES: Cancer- or chemotherapy-related cognitive deficit is a common side effect occurring in patients with Hodgkin lymphoma. No previous study compared the influence of different types of treatment on the onset and development of chemotherapy cognitive impairment in longitudinal design. The aim of this study was to assess whether a more intensive form of chemotherapy causes greater cognitive impairment. METHODS: Forty-four patients at three different stages of the disease and with three different treatments (ABVD + 30 Gy, BEACOPPesc, or ABVD + 30 Gy plus BEACOPPesc) completed the neuropsychological battery and psychological measures of affective distress and quality of life. We compared their cognitive performance before, immediately after, and 6 months after the treatment. RESULTS: Whether or not we divided the total number of people with Hodgkin lymphoma into two groups (mild and moderate disease versus severe disease) or three groups (mild, moderate, and advanced disease), we found no statistically significant difference between the groups in cognitive performance or other psychological factors or experienced quality of life. CONCLUSIONS: Our results did not show that disease stage or treatment protocol had an effect on the depth of cognitive impairment in cancer or chemotherapy. We hypothesize that, in terms of brain health, intensive forms of chemotherapy (6 × BEA-COPPesc) do not pose a greater risk than milder forms (4 × ABVD + 30 Gy IF RT and 2 × BEACOPPesc + 4 × ABVD + 30 Gy IF RT) of cancer treatment for Hodgkin lymphoma. However, a limitation of our study is the small number of participants in the study, so it would be advisable to repeat the study on a larger sample of patients. Confirmation of our results could be beneficial in that neither patients nor physicians need to worry that intensive chemotherapy will worsen cognitive deficits.
- Klíčová slova
- Hodgkin lymphoma, cancer, cancer-related cognitive impairment, chemotherapy, chemotherapy-related cognitive impairment, cognitive functions,
- Publikační typ
- časopisecké články MeSH
DNA methylation changes consistently throughout life and age-dependent alterations in DNA methylation can be used to estimate one's epigenetic age. Post-mortem studies revealed higher epigenetic age in brains of patients with major depressive disorder, as compared with controls. Since MDD is highly correlated with anxiety, we hypothesized that symptoms of anxiety, as well as lower volume of grey matter (GM) in depression-related cortical regions, will be associated with faster epigenetic clock in a community-based sample of young adults. Participants included 88 young adults (53% men; 23-24 years of age) from the European Longitudinal Study of Pregnancy and Childhood (ELSPAC) who participated in its neuroimaging follow-up and provided saliva samples for epigenetic analysis. Epigenetic age was calculated according to Horvath (Horvath, 2013). Women had slower epigenetic clock than men (Cohen's d = 0.48). In women (but not men), slower epigenetic clock was associated with less symptoms of anxiety. In the brain, women (but not men) with slower epigenetic clock had greater GM volume in the cerebral cortex (brain size-corrected; R2 = 0.07). Lobe-specific analyses showed that in women (but not men), slower epigenetic clock was associated with greater GM volume in frontal lobe (R2 = 0.16), and that GM volume in frontal lobe mediated the relationship between the speed of epigenetic clock and anxiety trait (ab = 0.15, SE = 0.15, 95% CI [0.007; 0.369]). These findings were not replicated, however, in a community-based sample of adolescents (n = 129; 49% men; 12-19 years of age), possibly due to the different method of tissue collection (blood vs. saliva) or additional sources of variability in the cohort of adolescents (puberty stages, socioeconomic status, prenatal exposure to maternal smoking during pregnancy).
- Klíčová slova
- Anxiety, DNA methylation age, Frontal lobe, Gray matter volume, Sex differences,
- MeSH
- depresivní porucha unipolární * MeSH
- dítě MeSH
- epigeneze genetická genetika MeSH
- lidé MeSH
- longitudinální studie MeSH
- magnetická rezonanční tomografie MeSH
- mladiství MeSH
- mladý dospělý MeSH
- šedá hmota MeSH
- těhotenství MeSH
- úzkost genetika MeSH
- úzkostné poruchy MeSH
- Check Tag
- dítě MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH