Parasites lost: using natural history collections to track disease change across deep time

Recent decades have brought countless outbreaks of infectious disease among wildlife. These events appear to be increasing in frequency and magnitude, but to objectively evaluate whether ecosystems are experiencing rising rates of disease, scientists require historical data on disease abundance. Specimens held in natural history collections represent a chronological archive of life on Earth and may, in many cases, be the only available source of data on historical disease patterns. It is possible to extract information on past disease rates by studying trace fossils (indirect fossilized evidence of an organism's presence or activity, including coprolites or feces), sequencing ancient DNA of parasites, and examining sediment samples, mummified remains, study skins (preserved animal skins prepared by taxidermy for research purposes), liquid‐preserved hosts, and hosts preserved in amber. Such use of natural history collections could expand scientific understanding of parasite responses to environmental change across deep time (that is, over the past several centuries), facilitating the development of baselines for managing contemporary wildlife disease.© The Ecological Society of America. The Author may post the work in a publicly accessible form on his/her personal or home institution's webpages. Full text available 10.1002/fee.2017. The attached file is the published pdf

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