Predation drives complex eco-evolutionary dynamics in sexually selected traits

Predation plays a role in preventing the evolution of ever more complicated sexual displays, because such displays often increase an individual's predation risk. Sexual selection theory, however, omits a key feature of predation in modeling costs to sexually selected traits: Predation is density dependent. As a result of this density dependence, predator-prey dynamics should feed back into the evolution of sexual displays, which, in turn, feeds back into predator-prey dynamics. Here, we develop both population and quantitative genetic models of sexual selection that explicitly link the evolution of sexual displays with predator-prey dynamics. Our primary result is that predation can drive eco-evolutionary cycles in sexually selected traits. We also show that mechanistically modeling the cost to sexual displays as predation leads to novel outcomes such as the maintenance of polymorphism in sexual displays and alters ecological dynamics by muting prey cycles. These results suggest predation as a potential mechanism to maintain variation in sexual displays and underscore that short-term studies of sexual display evolution may not accurately predict long-run dynamics. Further, they demonstrate that a common verbal model (that predation limits sexual displays) with widespread empirical support can result in unappreciated, complex dynamics due to the density-dependent nature of predation

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

Pervasive cortical and white matter anomalies in a mouse model for CHARGE syndrome

CHARGE (Coloboma of the eye, Heart defects, Atresia of the choanae, Retardation of growth, Genital anomalies and Ear abnormalities) syndrome is a disorder caused by mutations in the gene encoding CHD7, an ATP dependent chromatin remodelling factor, and is characterised by a diverse array of congenital anomalies. These include a range of neuroanatomical comorbidities which likely underlie the varied neurodevelopmental disorders associated with CHARGE syndrome, which include intellectual disability, motor coordination deficits, executive dysfunction, and autism spectrum disorder. Cranial imaging studies are challenging in CHARGE syndrome patients, but high-throughput magnetic resonance imaging (MRI) techniques in mouse models allow for the unbiased identification of neuroanatomical defects. Here, we present a comprehensive neuroanatomical survey of a Chd7 haploinsufficient mouse model of CHARGE syndrome. Our study uncovered widespread brain hypoplasia and reductions in white matter volume across the brain. The severity of hypoplasia appeared more pronounced in posterior areas of the neocortex compared to anterior regions. We also perform the first assessment of white matter tract integrity in this model through diffusion tensor imaging (DTI) to assess the potential functional consequences of widespread reductions in myelin, which suggested the presence of white matter integrity defects. To determine if white matter alterations correspond to cellular changes, we quantified oligodendrocyte lineage cells in the postnatal corpus callosum, uncovering reduced numbers of mature oligodendrocytes. Together, these results present a range of promising avenues of focus for future cranial imaging studies in CHARGE syndrome patients.</p