Abstract
The human brain’s ability to store information and remember past events is thought to be orchestrated by the synchronization of neuronal oscillations in various frequency bands. A vast amount of research has found that neural oscillations in the theta (∼4–7 Hz) and alpha (∼8–12 Hz) bands play an important role in memory formation. More specifically, it has been suggested that memory performance benefits if the same oscillatory pattern is present during encoding and retrieval. However, the causal relevance of these oscillations is not well understood. Rhythmic sensory stimulation is thought to entrain ongoing brain oscillations and modulate associated functions (e.g., memory formation). In the present study, we used rhythmic visual stimulation at 6 and 10 Hz to experimentally modulate the memory encoding process in a recognition memory task. In addition, we reinstated oscillatory activity from the encoding episode during retrieval, which has been hypothesized to result in memory performance improvements compared to non-reinstated conditions and incongruent reinstatement. Contrary to our hypothesis, we find no effect of neural entrainment during encoding on subsequent memory performance. Likewise, memory retrieval does not benefit from neural reinstatement. The results are discussed with respect to methodological challenges of rhythmic sensory stimulation as a means to alter cognitive processes and induce context-dependent memory effects.
Highlights
Red blood cells (RBCs), known as erythrocytes, are packed with hemoglobin tetramers and circulate throughout the body to supply all tissues with oxygen
Adult RBCs primarily contain adult hemoglobin (HbA), which consists of two copies of a-globin and two copies of b-globin. b-Thalassemic genetic disorders are caused by disruption of b-globin expression, causing loss of HbA and resulting in severe anemia, poor growth, and dramatically shortened lifespan. b-Thalassemia can be ameliorated by reexpression of g-globin, which complexes with a-globin to form fetal hemoglobin (HbF). g-Globin is normally expressed during development and silenced soon after birth, in an inverse relationship with b-globin
Loss of HBB Leads to Upregulation of g-Globin We previously observed that CRISPR-Cas9 editing at HBB in CD34+ mobilized peripheral blood hematopoietic stem and progenitor cells (HSPCs) induced g-globin transcription relative to unedited cells, leading to the formation of HbF tetramers (DeWitt et al, 2016)
Summary
Boontanrart et al model the cellular stress that occurs upon loss of b-globin in human erythroid cells. Decreased b-globin attenuates the eIF2aP-ATF4 pathway, resulting in increased fetal gglobin. ATF4 regulates the MYB g-globin repressor via binding at the HBS1L-MYB intergenic enhancer. August 4, 2020 a 2020 The Authors.
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