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Finding a bottle of milk in the bathroom would probably be quite surprising to most of us. Such a surprised reaction is driven by our strong expectations, learned through experience, that a bottle of milk belongs in the kitchen. Our environment is not randomly organized but governed by regularities that allow us to predict what objects can be found in which types of scene. These scene semantics are thought to play an important role in the recognition of objects. But when during development are the semantic predictions so far implemented that such scene-object inconsistencies would lead to semantic processing difficulties? Here we investigated how toddlers perceive their environments, and what expectations govern their attention and perception. To this aim, we used a purely visual paradigm in an ERP experiment and presented 24-month-olds with familiar scenes in which either a semantically consistent or an inconsistent object would appear. The scene-inconsistency effect has been previously studied in adults by means of the N400, a neural marker responding to semantic inconsistencies across many types of stimuli. Our results show that semantic object-scene inconsistencies indeed elicited an enhanced N400 over the left anterior brain region between 750 and 1150 ms post stimulus onset. This modulation of the N400 marker provides first indications that by the age of two toddlers have already established their scene semantics allowing them to detect a purely visual, semantic object-scene inconsistency. Our data suggest the presence of specific semantic knowledge regarding what objects occur in a certain scene category.
Considering the microbiome in stress-related and neurodevelopmental trajectories to schizophrenia
(2020)
Early life adversity and prenatal stress are consistently associated with an increased risk for schizophrenia, although the exact pathogenic mechanisms linking the exposures with the disease remain elusive. Our previous view of the HPA stress axis as an elegant but simple negative feedback loop, orchestrating adaptation to stressors among the hypothalamus, pituitary, and adrenal glands, needs to be updated. Research in the last two decades shows that important bidirectional signaling between the HPA axis and intestinal mucosa modulates brain function and neurochemistry, including effects on glucocorticoid hormones and brain-derived neurotrophic factor (BDNF). The intestinal microbiome in earliest life, which is seeded by the vaginal microbiome during delivery, programs the development of the HPA axis in a critical developmental window, determining stress sensitivity and HPA function as well as immune system development. The crosstalk between the HPA and the Microbiome Gut Brain Axis (MGBA) is particularly high in the hippocampus, the most consistently disrupted neural region in persons with schizophrenia. Animal models suggest that the MGBA remains influential on behavior and physiology across developmental stages, including the perinatal window, early childhood, adolescence, and young adulthood. Understanding the role of the microbiome on critical risk related stressors may enhance or transform of understanding of the origins of schizophrenia and offer new approaches to increase resilience against stress effects for preventing and treating schizophrenia.
The production of haploid gametes through meiosis is central to the principle of sexual reproduction. The genetic diversity is further enhanced by exchange of genetic material between homologous chromosomes by the crossover mechanism. This mechanism not only requires correct pairing of homologous chromosomes but also efficient repair of the induced DNA double-strand breaks. Oocytes have evolved a unique quality control system that eliminates cells if chromosomes do not correctly align or if DNA repair is not possible. Central to this monitoring system that is conserved from nematodes and fruit fly to humans is the p53 protein family, and in vertebrates in particular p63. In mammals, oocytes are stored for a long time in the prophase of meiosis I which, in humans, can last more than 50 years. During the entire time of this arrest phase, the DNA damage checkpoint remains active. The treatment of female cancer patients with DNA damaging irradiation or chemotherapeutics activates this checkpoint and results in elimination of the oocyte pool causing premature menopause and infertility. Here, we review the molecular mechanisms of this quality control system and discuss potential therapeutic intervention for the preservation of the oocyte pool during chemotherapy.