COVID-19 leads to severe respiratory problems, but also to long-COVID syndrome associated primarily with cognitive dysfunction and fatigue. Long-COVID syndrome symptoms, especially brain fog, are similar to those experienced by patients undertaking or following chemotherapy for cancer (chemofog or chemobrain), as well in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or mast cell activation syndrome (MCAS). The pathogenesis of brain fog in these illnesses is presently unknown but may involve neuroinflammation via mast cells stimulated by pathogenic and stress stimuli to release mediators that activate microglia and lead to inflammation in the hypothalamus. These processes could be mitigated by phytosomal formulation (in olive pomace oil) of the natural flavonoid luteolin.

Alzheimer's disease (AD), already the world's most common form of dementia, is projected to continue increasing in prevalence over the next several decades. The current lack of understanding of the pathogenesis of AD has hampered the development of effective treatments. Historically, AD research has been predicated on the amyloid cascade hypothesis (ACH), which attributes disease progression to the build-up of amyloid protein. However, multiple clinical studies of drugs interfering with ACH have failed to show any benefit demonstrating that AD etiology is more complex than previously thought. Here we review the current literature on the emerging key role of neuroinflammation, especially activation of microglia, in AD pathogenesis. Moreover, we provide compelling evidence that certain flavonoids, especially luteolin formulated in olive pomace oil together with hydroxytyrosol, offers a reasonable prophylactic treatment approach due to its many beneficial actions.

Little is known about the risk of COVID-19 infection among footballers. We aimed to investigate the incidence and characteristics of COVID-19 infection among footballers. In total, 480 football players of Super League Greece and 420 staff members participated in a prospective cohort study, which took place from May 2020 to May 2021. Nasopharyngeal swabs were collected from footballers and staff members weekly. All samples (n = 43,975) collected were tested using the reverse transcriptase polymerase chain reaction (RT-PCR) test for the detection of “SARS-CoV-2”. In total, 190 positive cases (130 among professional football players and 60 among staff) were recorded. Out of the 190 cases that turned positive, 64 (34%) cases were considered as symptomatic, and 126 (66%) cases were asymptomatic. The incidence rate of a positive test result for footballers was 0.57% (confidence interval (CI) 0.48–0.68%) and for staff members it was 0.27% (CI 0.20%, 0.34%), respectively. Footballers recorded a twofold increased risk of COVID-19 infection in comparison to staff members (relative risk = 2.16; 95% CI = 1.59–2.93; p-value < 0.001). No significant transmission events were observed during the follow-up period. We found a low incidence of COVID-19 infection among professional footballers over a long follow-up period. Furthermore, the implementation of a weekly diagnostic testing (RT-PCR) was critical to break the transmission chain of COVID-19, especially among asymptomatic football players and staff members.

Chronic kidney disease (CKD) is an important global public health problem due to its high prevalence and morbidity. Although the treatment of nephrology patients has changed considerably, ineffectiveness and side effects of medications represent a major issue. In an effort to elucidate the contribution of genetic variants located in several genes in the response to treatment of patients with CKD, we performed a systematic review and meta-analysis of all available pharmacogenetics studies. The association between genotype distribution and response to medication was examined using the dominant, recessive, and additive inheritance models. Subgroup analysis based on ethnicity was also performed. In total, 29 studies were included in the meta-analysis, which examined the association of 11 genes (16 polymorphisms) with the response to treatment regarding CKD. Among the 29 studies, 18 studies included patients with renal transplantation, 8 involved patients with nephrotic syndrome, and 3 studies included patients with lupus nephritis. The present meta-analysis provides strong evidence for the contribution of variants harbored in the ABCB1, IL-10, ITPA, MIF, and TNF genes that creates some genetic predisposition that reduces effectiveness or is associated with adverse events of medications used in CKD.