In mid-December 2019, a novel atypical pneumonia broke out in Wuhan, Hubei Province, China and was caused by a newly identified coronavirus, initially termed 2019 Novel Coronavirus and subsequently severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As of 19 May 2020, a total of 4,731,458 individuals were reported as infected with SARS-CoV-2 among 213 countries, areas or territories with recorded cases, and the overall case-fatality rate was 6.6% (316,169 deaths among 4,731,458 recorded cases), according to the World Health Organization. Studies have shown that SARS-CoV-2 is notably similar to (severe acute respiratory syndrome coronavirus) SARS-CoV that emerged in 2002–2003 and Middle East respiratory syndrome coronavirus (MERS-CoV) that spread during 2012, and these viruses all contributed to global pandemics. The ability of SARS-CoV-2 to rapidly spread a pneumonia-like disease from Hubei Province, China, throughout the world has provoked widespread concern. The main symptoms of coronavirus disease 2019 (COVID-19) include fever, cough, myalgia, fatigue and lower respiratory signs. At present, nucleic acid tests are widely recommended as the optimal method for detecting SARS-CoV-2. However, obstacles remain, including the global shortage of testing kits and the presentation of false negatives. Experts suggest that almost everyone in China is susceptible to SARS-CoV-2 infection, and to date, there are no effective treatments. In light of the references published, this review demonstrates the biological features, spread, diagnosis and treatment of SARS-CoV-2 as a whole and aims to analyse the similarities and differences among SARS-CoV-2, SARS-CoV and MERS-CoV to provide new ideas and suggestions for prevention, diagnosis and clinical treatment.

Autism spectrum disorders (ASDs) are a kind of neurodevelopmental disorder with rapidly increasing morbidity. In recent years, many studies have proposed a possible link between ASD and multiple environmental as well as genetic risk factors; nevertheless, recent studies have still failed to identify the specific pathogenesis. An analysis of the literature showed that oxidative stress and redox imbalance caused by high levels of reactive oxygen species (ROS) are thought to be integral parts of ASD pathophysiology. On the one hand, this review aims to elucidate the communications between oxidative stress, as a risk factor, and ASD. As such, there is also evidence to suggest that early assessment and treatment of antioxidant status are likely to result in improved long-term prognosis by disturbing oxidative stress in the brain to avoid additional irreversible brain damage. Accordingly, we will also discuss the possibility of novel therapies regarding oxidative stress as a target according to recent literature. On the other hand, this review suggests a definite relationship between ASD and an unbalanced gastrointestinal tract (GIT) microbiota (i.e., GIT dysbiosis). A variety of studies have concluded that the intestinal microbiota influences many aspects of human health, including metabolism, the immune and nervous systems, and the mucosal barrier. Additionally, the oxidative stress and GIT dysfunction in autistic children have both been reported to be related to mitochondrial dysfunction. What is the connection between them? Moreover, specific changes in the GIT microbiota are clearly observed in most autistic children, and the related mechanisms and the connection among ASD, the GIT microbiota, and oxidative stress are also discussed, providing a theory and molecular strategies for clinical practice as well as further studies.

Alzheimer’s disease (AD) is a multi-factorial neurodegenerative disorder with abnormal accumulation of amyloid-β (Aβ) plaques, neuroinflammation and impaired neurogenesis. Mounting evidences suggest that single-target drugs have limited effects on clinical treatment and alternative or multiple targets are required. In recent decades, natural compounds and their derivatives have gained increasing attention in AD drug discovery due to their inherently enormous chemical and structural diversity. In this study, we demonstrated that naringin dihydrochalcone (NDC), a widely used dietary sweetener with strong antioxidant activity, improved the cognitive function of transgenic AD mice. Pathologically, NDC attenuated Aβ deposition in AD mouse brain. Furthermore, NDC reduced periplaque activated microglia and astrocytes, indicating the inhibition of neuroinflammation. It also enhanced neurogenesis as investigated by BrdU/NeuN double labeling. Additionally, the inhibition of Aβ level and neuroinflammation by NDC treatment was also observed in an AD cell model or a microglia cell line. Taken together, our study indicated that NDC might be a potential therapeutic agent for the treatment of AD against multiple targets that include Aβ pathology, neuroinflammation and neurogenesis.