Switching memory perspective

The perspective in which memories were spontaneously recalled, field (original perspective) or observer (see oneself in the memory), was examined for both recent and remote memories. Recent memories were dominated by field perspective whilst remote memories were dominated by observer perspective. Further, field memories contained reliably more episodic detail than observer memories. After a 1-week interval, the same memories were recalled again but with a switched memory perspective. Switching from an observer to a field perspective did not reliably increase the amount of episodic details in a memory. Switching from field to observer perspective did, however, reliably reduce the number of episodic details. These findings suggest that memories may be represented in long-term memory with a fixed perspective, either field or observer, which can be temporarily altered sometimes changing the nature of a memory, i.e. how much detail remains accessible

Fictional first memories

YesIn a large-scale survey, 6,641 respondents provided descriptions of their first memory and their age when they encoded that memory, and they completed various memory judgments and ratings. In good agreement with many other studies, where mean age at encoding of earliest memories is usually found to fall somewhere in the first half of the 3rd year of life, the mean age at encoding here was 3.2 years. The established view is that the distribution around mean age at encoding is truncated, with very few or no memories dating to the preverbal period, that is, below about 2 years of age. However, we found that 2,487 first memories (nearly 40% of the entire sample) dated to an age at encoding of 2 years and younger, with 893 dating to 1 year and younger. We discuss how such improbable, fictional first memories could have arisen and contrast them with more probable first memories, those with an age at encoding of 3 years and older

True and intentionally fabricated memories

The aim of the experiment reported here was to investigate the processes underlying the construction of truthful and deliberately fabricated memories. Properties of memories created to be intentionally false - fabricated memories - were compared to properties of memories believed to be true - true memories. Participants recalled and then wrote or spoke true memories and fabricated memories of everyday events. It was found that true memories were reliably more vivid than fabricated memories and were nearly always recalled from a first person perspective. In contrast, fabricated differed from true memories in that they were judged to be reliably older, were more frequently recalled from a third person perspective, and linguistic analysis revealed that they required more cognitive effort to generate. No notable differences were found across modality of reporting. Finally, it was found that, intentionally fabricated memories were created by recalling and then ‘editing’ true memories. Overall, these findings show that true and fabricated memories systematically differ, despite the fact that both are based on true memories

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

A saturated map of common genetic variants associated with human height

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries

A saturated map of common genetic variants associated with human height.

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes <sup>1</sup> . Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel <sup>2</sup> ) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries