Principles for designing marine protected area (MPA) networks that address social, economic, and biological criteria are well established in the scientific literature. Climate change represents a new and serious threat to marine ecosystems, but, to date, few studies have specifically considered how to design MPA networks to be resilient to this emerging threat. Here, we compile the best available information on MPA network design and supplement it with specific recommendations for building resilience into these networks. We provide guidance on size, spacing, shape, risk spreading (representation and replication), critical areas, connectivity, and maintaining ecosystem function to help MPA planners and managers design MPA networks that are more robust in the face of climate‐change impacts.

SignificanceMarine reserves that prohibit fishing are a critical tool for sustaining coral reef ecosystems, yet it remains unclear how human impacts in surrounding areas affect the capacity of marine reserves to deliver key conservation benefits. Our global study found that only marine reserves in areas of low human impact consistently sustained top predators. Fish biomass inside marine reserves declined along a gradient of human impacts in surrounding areas; however, reserves located where human impacts are moderate had the greatest difference in fish biomass compared with openly fished areas. Reserves in low human-impact areas are required for sustaining ecological functions like high-order predation, but reserves in high-impact areas can provide substantial conservation gains in fish biomass.

A global survey of reef fishes shows that the consequences of biodiversity loss are greater than previously anticipated as ecosystem functioning remained unsaturated with the addition of new species. Additionally, reefs worldwide, particularly those most diverse, are highly vulnerable to human impacts that are widespread and likely to worsen due to ongoing coastal overpopulation.

Sporadic Creutzfeldt-Jakob disease (sCJD) is a fatal and potentially transmissible neurodegenerative disease caused by misfolded prion proteins. To date, effective therapeutics are not available and accurate diagnosis can be challenging. Clinical diagnostic criteria employ a combination of characteristic cerebrospinal fluid (CSF) 14-3-3 proteins, MRI findings, EEG changes, and neuropsychiatric symptoms. Supportive biomarkers such as high CSF total Tau may aid the diagnostic process. However, discordant results of studies have led to controversies about the clinical value of established surrogate biomarkers. The recent development and clinical application of disease-specific protein aggregation and amplification assays such as Real-time Quaking Induced Conversion (RT-QuIC) have constituted major breakthroughs for the confident pre-mortem diagnosis of sCJD. Updated criteria for the biomarker-based diagnosis of sCJD including RT-QuIC will improve early clinical confirmation, disease surveillance, assessment of potential tissue infectivity, and trial monitoring. Further, potential pre-symptomatic, prognostic, and blood-based biomarker candidates have been identified in recent years.

No abstract