Aging and neurodegenerative diseases share oxidative stress cell damage and depletion of endogenous antioxidants as mechanisms of injury, phenomena that are occurring at different rates in each process. Nevertheless, as the central nervous system (CNS) consists largely of lipids and has a poor catalase activity, a low amount of superoxide dismutase and is rich in iron, its cellular components are damaged easily by overproduction of free radicals in any of these physiological or pathological conditions. Thus, antioxidants are needed to prevent the formation and to oppose the free radicals damage to DNA, lipids, proteins, and other biomolecules. Due to endogenous antioxidant defenses are inadequate to prevent damage completely, different efforts have been undertaken in order to increase the use of natural antioxidants and to develop antioxidants that might ameliorate neural injury by oxidative stress. In this context, natural antioxidants like flavonoids (quercetin, curcumin, luteolin and catechins), magnolol and honokiol are showing to be the efficient inhibitors of the oxidative process and seem to be a better therapeutic option than the traditional ones (vitamins C and E, and β-carotene) in various models of aging and injury in vitro and in vivo conditions. Thus, the goal of the present review is to discuss the molecular basis, mechanisms of action, functions, and targets of flavonoids, magnolol, honokiol and traditional antioxidants with the aim of obtaining better results when they are prescribed on aging and neurodegenerative diseases.

Dermatophyte infections are the most common fungal infections in humans; among them, tinea capitis (TC) – the most contagious fungal infection – is caused by anthropophilic, zoophilic and geophilic dermatophytes. The purpose of this systematic review was to determine the different aetiological variants involved in TC and the overall epidemiology of the causes of this infection in the last two decades. We searched the MEDLINE (PubMed) and Embase databases for articles published from July 2000 to August 2019 using the following search terms: ‘Tinea capitis’, ‘Africa’, ‘America’, ‘Asia’, ‘Europe’, ‘Oceania’, and the names of the countries on each continent. The flow of information through the different phases in this systematic review was depicted using a PRISMA flow diagram, which mapped the number of records identified, included and excluded, and the reasons for exclusion. Our findings indicate that the frequency of different aetiologic agents of TC in the reported studies varied globally, from 0.4–87.7% in Africa, 0.2–74.0% in North America, 0.0–91.2% in Eastern Asia, 0.0–69.0% in Eastern Europe and 2.9–86.4% in Oceania. Microsporum canis is the most frequent reported zoophilic agent worldwide, while Trichophyton violaceum and Trichophyton tonsurans are the predominant anthropophilic agents. Over time, the frequency of these latter fungal infections has increased globally, and these fungi have become the major species globally. Anthropophilic transmission – the most prevalent type of transmission – could be explained by two factors: (i) the socioeconomic status of affected countries and population groups with associated risk factors and (ii) movement of populations importing new causes of infection to areas where they had not been encountered previously. We observed that intercontinental migration and travel; globalization; environmental, climatic and ecological changes; and accelerated evolution of health technologies may influence the observed epidemiological changes and, consequently, contributed to the variations in the global status of TC.

Several growth factors, such as vascular endothelial growth factor, brain-derived neurotrophic factor, and insulin-like growth factor-I are involved in the actions of progesterone in the central nervous system. Previous studies in neuronal and glial cultures have shown that progesterone may regulate growth factor signaling, increasing the phosphorylation of extracellular-signal regulated kinase (ERK) and the phosphorylation of Akt, components of the mitogen-activated protein kinase (MAPK) and the phosphoinositide-3 kinase (PI3K) signaling pathways, respectively. In this study, we have evaluated whether progesterone and its reduced metabolites, dihydroprogesterone and tetrahydroprogesterone, regulate PI3K and MAPK signaling in the brain of ovariectomized rats in vivo. Significant increases in the phosphorylation of ERK, in the expression of the catalytic (p110) and the regulatory (p85) subunits of PI3K and in the phosphorylation of Akt were observed in the hypothalamus, the hippocampus, and the cerebellum 24 hr after progesterone administration. Progesterone metabolites partially mimicked the effect of progesterone and had a stronger effect on MAPK and PI3K signaling in the hypothalamus than in the other brain regions. These findings suggest that progesterone regulates MAPK and PI3K signaling pathways in the central nervous system in vivo by direct hormonal actions and by mechanisms involving progesterone metabolites.