Camtrap DP: an open standard for the FAIR exchange and archiving of camera trap data

Camera trapping has revolutionized wildlife ecology and conservation by providing automated data acquisition, leading to the accumulation of massive amounts of camera trap data worldwide. Although management and processing of camera trap-derived Big Data are becoming increasingly solvable with the help of scalable cyber-infrastructures, harmonization and exchange of the data remain limited, hindering its full potential. There is currently no widely accepted standard for exchanging camera trap data. The only existing proposal, “Camera Trap Metadata Standard” (CTMS), has several technical shortcomings and limited adoption. We present a new data exchange format, the Camera Trap Data Package (Camtrap DP), designed to allow users to easily exchange, harmonize and archive camera trap data at local to global scales. Camtrap DP structures camera trap data in a simple yet flexible data model consisting of three tables (Deployments, Media and Observations) that supports a wide range of camera deployment designs, classification techniques (e.g., human and AI, media-based and event-based) and analytical use cases, from compiling species occurrence data through distribution, occupancy and activity modeling to density estimation. The format further achieves interoperability by building upon existing standards, Frictionless Data Package in particular, which is supported by a suite of open software tools to read and validate data. Camtrap DP is the consensus of a long, in-depth, consultation and outreach process with standard and software developers, the main existing camera trap data management platforms, major players in the field of camera trapping and the Global Biodiversity Information Facility (GBIF). Under the umbrella of the Biodiversity Information Standards (TDWG), Camtrap DP has been developed openly, collaboratively and with version control from the start. We encourage camera trapping users and developers to join the discussion and contribute to the further development and adoption of this standard

Modeling psychiatric disorders: from genomic findings to cellular phenotypes

Major programs in psychiatric genetics have identified 4150 risk loci for psychiatric disorders. These loci converge on a small number of functional pathways, which span conventional diagnostic criteria, suggesting a partly common biology underlying schizophrenia, autism and other psychiatric disorders. Nevertheless, the cellular phenotypes that capture the fundamental features of psychiatric disorders have not yet been determined. Recent advances in genetics and stem cell biology offer new prospects for cell-based modeling of psychiatric disorders. The advent of cell reprogramming and induced pluripotent stem cells (iPSC) provides an opportunity to translate genetic findings into patient-specific in vitro models. iPSC technology is less than a decade old but holds great promise for bridging the gaps between patients, genetics and biology. Despite many obvious advantages, iPSC studies still present multiple challenges. In this expert review, we critically review the challenges for modeling of psychiatric disorders, potential solutions and how iPSC technology can be used to develop an analytical framework for the evaluation and therapeutic manipulation of fundamental disease processes

Epigenetic mechanisms during ageing and neurogenesis as novel therapeutic avenues in human brain disorders

Abstract Ageing is the main risk factor for human neurological disorders. Among the diverse molecular pathways that govern ageing, epigenetics can guide age-associated decline in part by regulating gene expression and also through the modulation of genomic instability and high-order chromatin architecture. Epigenetic mechanisms are involved in the regulation of neural differentiation as well as in functional processes related to memory consolidation, learning or cognition during healthy lifespan. On the other side of the coin, many neurodegenerative diseases are associated with epigenetic dysregulation. The reversible nature of epigenetic factors and, especially, their role as mediators between the genome and the environment make them exciting candidates as therapeutic targets. Rather than providing a broad description of the pathways epigenetically deregulated in human neurological disorders, in this review, we have focused on the potential use of epigenetic enzymes as druggable targets to ameliorate neural decline during normal ageing and especially in neurological disorders. We will firstly discuss recent progress that supports a key role of epigenetic regulation during healthy ageing with an emphasis on the role of epigenetic regulation in adult neurogenesis. Then, we will focus on epigenetic alterations associated with ageing-related human disorders of the central nervous system. We will discuss examples in the context of psychiatric disorders, including schizophrenia and posttraumatic stress disorders, and also dementia or Alzheimer’s disease as the most frequent neurodegenerative disease. Finally, methodological limitations and future perspectives are discussed