Corrigendum: Methylmercury impact on adult neurogenesis: is the worst yet to come from recent Brazilian environmental disasters?

[This corrects the article DOI: 10.3389/fnagi.2020.591601.].

High-Intense Interval Training Prevents Cognitive Impairment And Increases The Expression Of Muscle Genes Fndc5 And Ppargc1a In A Rat Model Of Alzheimer's Disease.

BACKGROUND: Alzheimer's disease is the most common neurodegenerative disease in the world, characterized by the progressive loss of neuronal structure and function, whose main histopathological landmark is the accumulation of ß-amyloid in the brain. OBJECTIVE: It is well known that exercise is a neuroprotective factor and that muscles produce and release myokines that exert endocrine effects in inflammation and metabolic dysfunction. Thus, this work intends to establish the relationship between the benefits of exercise through the chronic training of HIIT on cognitive damage induced by the Alzheimer's model by the injection of ß amyloid 1-42. METHODS: For this purpose, forty-eight male Wistar rats were divided into four groups: Sedentary Sham (SS), Trained Sham (ST), Sedentary Alzheimer's (AS), and Trained Alzheimer's (AT). Animals were submitted to stereotactic surgery and received a hippocampal injection of Aß1-42 or a saline solution. Seven days after surgery, twelve days of treadmill adaptation followed by five maximal running tests (MRT) and fifty-five days of HIIT, rats underwent the Morris water maze test. The animals were then euthanized, and their gastrocnemius muscle tissue was extracted to analyze the Fibronectin type III domain containing 5 (FNDC5), PPARG Coactivator 1 Alpha (PPARGC1A), and Integrin subunit beta 5 (ITGB5-R) expression by qRT-PCR in addition to cross-sectional areas. RESULTS: The HIIT prevents the cognitive deficit induced by the infusion of amyloid ß 1-42 (p<0.0001), causes adaptation of muscle fibers (p<0.0001), modulates the gene expression of FNDC5 (p<0.01), ITGB5 (p<0.01) and PPARGC1A (p<0.01), and induces an increase in peripheral protein expression of FNDC5 (p<0.005). CONCLUSION: Thus, we conclude that HIIT can prevent cognitive damage induced by the infusion of Aß1-42, constituting a non-pharmacological tool that modulates important genetic and protein pathways.

Methylmercury Impact on Adult Neurogenesis: Is the Worst Yet to Come From Recent Brazilian Environmental Disasters?

Worldwide environmental tragedies of anthropogenic origin causing massive release of metals and other pollutants have been increasing considerably. These pollution outbreaks affect the ecosystems and impact human health. Among those tragedies, recent large-scale environmental disasters in Brazil strongly affected riverside populations, leading to high-risk exposure to methylmercury (MeHg). MeHg is highly neurotoxic to the developing brain. This toxicant causes neural stem cell dysfunction and neurodevelopmental abnormalities. However, less is known about the effects of MeHg in the postnatal neurogenic niche, which harbors neural stem cells and their progeny, in the adult brain. Therefore, taking in consideration the impact of MeHg in human health it is urgent to clarify possible associations between exposure to mercury, accelerated cognitive decline, and neurodegenerative diseases. In this perspectives paper, we discuss the neurotoxic mechanisms of MeHg on postnatal neurogenesis and the putative implications associated with accelerated brain aging and early-onset cognitive decline in populations highly exposed to this environmental neurotoxicant.

Pollutants and nutrition: Are methylmercury effects on blood pressure and lipoprotein profile comparable to high-fat diet in mice?

Human exposure to methylmercury (MeHg) due to contaminated fish intake as part of a high-fat (HFD), high-carbohydrate diets is a reality today for many populations. HFD is associated with hypertension and hyperlipidemia, primary cardiovascular disease (CVD) risk factors. Some studies suggest that MeHg induces those risk factors. We evaluated the effect of MeHg exposure in mice fed with HFD or control diet for eight weeks. In the last experimental 15 days, the half group received a MeHg solution (20 mg/L) replacing water. Blood pressure (BP), heart rate, lipoprotein concentrations, and paraoxonase activity were evaluated. Liver cholesterol, triacylglycerol, and IBA-1+ cells, as well as transcriptional levels of genes related to lipid metabolism and inflammatory response, were also assessed. HFD and both MeHg groups presented increased BP and total cholesterol (TC). In the liver, HFD but not MeHg was related to an increase in TC. Also, MeHg intoxication reduced paraoxonase activity regardless of diet. MeHg intoxication and HFD increased steatosis and the number of IBA-1+ cells and modified some gene transcripts associated with lipid metabolism. In conclusion, we demonstrated that MeHg effects on CVD risk factors resemble those caused by HFD.

Novel renal biomarkers show that creatine supplementation is safe: a double-blind, placebo-controlled randomized clinical trial.

The aim of this study was to evaluate the impact of creatine supplementation (CS) on renal function in young, healthy, and active subjects. We used a randomized, double-blind, placebo-controlled clinical trial as the study design. Thirty-six healthy male university students were recruited and divided into three groups: group placebo, group G3 (3 g/day of CS), and group G5 (5 g/day of CS). To assess renal function, new kidney biomarkers, kidney injury molecule-1 (KIM-1) and monocyte chemoattractant protein-1 (MCP-1), were quantified. Serum albumin, serum creatinine, serum urea, estimated glomerular filtration rate (eGFR), proteinuria, and albuminuria were also measured. All groups were evaluated at two times: prior CS or placebo (pre) and after 35 days on CS or placebo (post). After 35 days of intervention, all characteristics were maintained without significant difference (P > 0.05) between the groups, including serum creatinine, eGFR, and more sensitive kidney biomarker concentrations (KIM-1 and MCP-1). The paired analysis showed that the supplemented groups (G3 and 5G) had increased serum creatinine and decreased eGFR levels (P < 0.05). However, the values were still within the normal reference range. In conclusion, the results of renal function evaluation did not show any difference between the evaluated groups. Increased serum creatinine and decreased eGFR levels in CS groups can be explained by increased creatine stores and metabolism, since creatinine is a by-product of creatine metabolism. These findings indicate that the use of CS at doses of 3 g and 5 g/day for a short period (35 days) is safe and did not impair the kidneys or renal function in young healthy subjects.

Disorder of hypothalamic-pituitary-gonadal axis induced by abusing of anabolic-androgenic steroids for short time: A case report.

The aim of this study was to evaluate the hypothalamic-pituitary-gonadal axis functionality on a bodybuilding competitioner before, during and after the use of anabolic-androgenic steroids. A young healthy man was followed up for 4 months. The subject reported his drug administration protocol through periodic interviews and performed laboratory tests to monitor the function of his hypothalamic-pituitary-gonadal axis. Time 1 (before the steroids use) shows all hormones levels (follicle-stimulating hormone = 4,2 mUI/ml, luteinising hormone = 3,7 mUI/ml and total testosterone = 5,7 ng/ml) within reference values. In Time 2, after 8 weeks on steroids abuse, a complete hypothalamic-pituitary-gonadal axis derangement is evident with noticeable negative feedback (follicle-stimulating hormone = 1,47 mUI/ml, luteinising hormone = 0,1 mUI/ml and total testosterone = 1,47 ng/ml). At the third moment (40 days after Time 2), we can see a tendency to recovery, however, the serum levels of the investigated hormones were still considerably lower than the baseline values. At the end, we could conclude that the use of anabolic-androgenic steroids, at supraphysiological dosages, even for a short time (8 weeks), causes severe disorder in the hypothalamic-pituitary-gonadal axis. The endogenous testosterone synthesis was severely compromised by important decline in serum luteinising hormone levels.