The Pandemic of COVID-19, an infectious disease caused by SARS-CoV-2 motivated the scientific community to work together in order to gather, organize, process and distribute data on the novel biomedical hazard. Here, we analyzed how the scientific community responded to this challenge by quantifying distribution and availability patterns of the academic information related to COVID-19. The aim of this study was to assess the quality of the information flow and scientific collaboration, two factors we believe to be critical for finding new solutions for the ongoing pandemic. The RISmed R package, and a custom Python script were used to fetch metadata on articles indexed in PubMed and published on Rxiv preprint server. Scopus was manually searched and the metadata was exported in BibTex file. Publication rate and publication status, affiliation and author count per article, and submission-to-publication time were analysed in R. Biblioshiny application was used to create a world collaboration map. Preliminary data suggest that COVID-19 pandemic resulted in generation of a large amount of scientific data, and demonstrates potential problems regarding the information velocity, availability, and scientific collaboration in the early stages of the pandemic. More specifically, the results indicate precarious overload of the standard publication systems, significant problems with data availability and apparent deficient collaboration. In conclusion, we believe the scientific community could have used the data more efficiently in order to create proper foundations for finding new solutions for the COVID-19 pandemic. Moreover, we believe we can learn from this on the go and adopt open science principles and a more mindful approach to COVID-19-related data to accelerate the discovery of more efficient solutions. We take this opportunity to invite our colleagues to contribute to this global scientific collaboration by publishing their findings with maximal transparency.

Alzheimer’s disease (AD) is a neurodegenerative disorder with a growing epidemiological importance characterized by significant disease burden. Sleep-related pathological symptomatology often accompanies AD. The etiology and pathogenesis of disrupted circadian rhythm and AD share common factors, which also opens the perspective of viewing them as a mutually dependent process. This article focuses on the bi-directional relationship between these processes, discussing the pathophysiological links and clinical aspects. Common mechanisms linking both processes include neuroinflammation, neurodegeneration, and circadian rhythm desynchronization. Timely recognition of sleep-specific symptoms as components of AD could lead to an earlier and correct diagnosis with an opportunity of offering treatments at an earlier stage. Likewise, proper sleep hygiene and related treatments ought to be one of the priorities in the management of the patient population affected by AD. This narrative review brings a comprehensive approach to clearly demonstrate the underlying complexities linking AD and circadian rhythm disruption. Most clinical data are based on interventions including melatonin, but larger-scale research is still scarce. Following a pathophysiological reasoning backed by evidence gained from AD models, novel anti-inflammatory treatments and those targeting metabolic alterations in AD might prove useful for normalizing a disrupted circadian rhythm. By restoring it, benefits would be conferred for immunological, metabolic, and behavioral function in an affected individual. On the other hand, a balanced circadian rhythm should provide greater resilience to AD pathogenesis.

Non-antibiotic drugs can alter the composition of the gut microbiome¹, but they have largely unknown implications for human health². Here we examined how non-antibiotics affect the ability of gut commensals to resist colonization by enteropathogens³. We also developed an in vitro assay to assess enteropathogen growth in drug-perturbed microbial communities. Pathogenic Gammaproteobacteria were more resistant to non-antibiotics than commensals and their post-treatment expansion was potentiated. For 28% of the 53 drugs tested, the growth of Salmonella enterica subsp. enterica serovar Typhimurium. (S. Tm) in synthetic and human stool-derived communities was increased, and similar effects were observed for other enteropathogens. Non-antibiotics promoted pathogen proliferation by inhibiting the growth of commensals, altering microbial interactions and enhancing the ability of S. Tm to exploit metabolic niches. Drugs that promoted pathogen expansion in vitro increased the intestinal S. Tm load in mice. For the antihistamine terfenadine, drug-induced disruption of colonization resistance accelerated disease onset and increased inflammation caused by S. Tm. Our findings identify non-antibiotics as previously overlooked risk factors that may contribute to the development of enteric infections.