Search

Zika virus (ZIKV) infection during the pregnancy period is related to microcephaly and neurobehavioral disorders at birth, while prenatal exercise is supposed to provide neuroprotection in newborns pups. The aim of this study was to investigate the neurological consequences of exercise during prenatal ZIKV exposure to mice pups. Twelve weeks female mice were randomly assigned into three groups: Control group, intraperitoneally injected with saline (Control); untrained group, intraperitoneally injected with ZIKV (ZIKV); and trained group, intraperitoneally injected with ZIKV (ZIKV/swim). There was one familiarization week prior to the beginning of the swimming training. Dams swam for 60 min/session, 5 days/week, during 4 weeks. Mating occurred between the fifth and seventh day of the first week of the swimming training. ZIKV 106 plaque-forming units/100 µl (106 PFUs/100 µl) or an equal volume of saline was intraperitoneally injected in the pregnant mice at embryonic day 10.5. Pup's body mass and brain weight were measured at postnatal day 1 (P1). Behavioral tests were performed from P30 to P35. Thereafter, hippocampal levels of syntaxin-1, GFAP, IBA-1, and BDNF were measured. Exercise during prenatal ZIKV exposure prevented brain atrophy, development of depression, anxiety, and disruption of social behavior. Exercise during prenatal ZIKV exposure inhibited the overexpression of microglia (IBA-1) and astrocytes (GFAP), with reduction of BDNF levels in the hippocampi of female and male mice pups. No significant changes were seen in syntaxin-1 levels. Our findings reveal beneficial effects of exercise during pregnancy exposure to ZIKV in mice pups. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disease, and its prevalence has grown worldwide. Several pathophysiological processes contribute to the development, progression and aggravating of the disease, for example, decreased insulin synthesis and secretion, insulin resistance, inflammation, and apoptosis, all these processes are regulated by various epigenetic factors, including microRNAs (miRNAs). MiRNAs are small non-coding RNAs, which are around 20 nucleotides in length and are regulators of gene expression at the post-transcriptional level, have a specific function of inhibiting or degrading a messenger RNA target. Thus, miRNAs modulate the expression of many associated genes with the pathophysiological processes in T2DM. On the other hand, miRNAs are also modulated through physical exercise (PE), which induces a change in their expression pattern during and after exercise. Some scientific evidence shows that PE modulates miRNAs beneficially and improves the signaling pathway of insulin resistance, however, little is known about the function of PE modulating miRNAs associated with the processes of insulin secretion, inflammation, and apoptosis. Thus, the objective of this review is to identify the miRNAs expression pattern in T2DM and compare it with the exercise-induced miRNAs expression pattern, identifying the signaling pathways that these miRNAs are regulating in the processes of insulin secretion, insulin resistance, inflammation, and apoptosis in T2DM, and how PE may have a potential role in modulating these signal transduction pathways, promoting benefits for patients with T2DM. [ABSTRACT FROM AUTHOR]

• T2D main feature is insulin resistance, which is the hallmark of cognitive decline. • Resistance training is a non-pharmacological tool that ameliorates T2D features. • Locomotor activity or anxious behavior are not significantly altered in T2D rats. • T2D rats preserved cognition after 4 weeks of high-intensity resistance training. • T2D rats which did not perform resistance training presented cognitive impairment. Type 2 diabetes (T2D) is a metabolic disorder that can lead to cognitive decline through impairment of insulin signaling. Resistance training, a type of physical exercise, is a non-pharmacological approach used to improve insulin resistance in T2D. The aim of our study was to evaluate the effects of high-intensity resistance training (HIRT) over cognitive function, locomotor activity, and anxious behavior in rats induced to T2D. Thirty young adult male wistar rats were distributed into 3 groups (n = 10): Control; dexamethasone (D); and dexamethasone + exercise (DE), that performed the HIRT during 4 weeks. Blood glucose, water intake, and total body fat were measured. Locomotor activity, and anxious behavior where evaluated through the open field task. Cognitive function was assessed through the novel object recognition task. Insulin resistance and neuronal death were evaluated through western blot analysis. Rats induced to T2D had higher blood glucose levels, and consumed more water when compared to control group, but DE had better blood glucose levels than D. Total body fat was reduced in DE compared to D. Locomotor activity, and anxious behavior were not significantly altered. T2D rats which performed HIRT maintained cognitive function, while those induced to T2D that did not exercise developed cognitive decline. DE group showed a reduction in the inhibition of the activation of hippocampal IRS-1 and higher expression of GSk3β phosphorylated in serine compared to D group, revealing insulin signaling impairment, and neuronal death were identified in the hippocampus of D group. Lifestyle intervention through the regular practice of HIRT plays a fundamental role in the treatment of T2D preventing cognitive decline. [ABSTRACT FROM AUTHOR]

Alzheimer disease (AD) is one of the most common neurodegenerative diseases, affecting middle-aged and elderly individuals worldwide. AD pathophysiology involves the accumulation of beta-amyloid plaques and neurofibrillary tangles in the brain, along with chronic neuroinflammation and neurodegeneration. Physical exercise (PE) is a beneficial non-pharmacological strategy and has been described as an ally to combat cognitive decline in individuals with AD. However, the molecular mechanisms that govern the beneficial adaptations induced by PE in AD are not fully elucidated. MicroRNAs are small non-coding RNAs involved in the post-transcriptional regulation of gene expression, inhibiting or degrading their target mRNAs. MicroRNAs are involved in physiological processes that govern normal brain function and deregulated microRNA profiles are associated with the development and progression of AD. It is also known that PE changes microRNA expression profile in the circulation and in target tissues and organs. Thus, this review aimed to identify the role of deregulated microRNAs in the pathophysiology of AD and explore the possible role of the modulation of microRNAs as a molecular mechanism involved in the beneficial actions of PE in AD. [ABSTRACT FROM AUTHOR]

• Intense physical training is suggested to be harmful to cognitive function. • HIIT was used to assess redox state, behavior and cognitive function in rats. • HIIT did not change the anxious profile or locomotor activity. • Lipid peroxidation, and antioxidant mechanisms were seen in cerebellar tissue. • HIIT had no deleterious effects on rats' cognitive function. High-intensity interval training (HIIT) is associated with better physical performance, but there is limited information about the effects of HIIT on redox state of cerebellar tissue, cerebral cortex, and cognition. The aim of this study was to evaluate the effects of HIIT on redox state parameters in cerebellar tissue, cerebral cortex, and cognitive function of Wistar rats. Forty-three young male Wistar rats were housed under controlled environmental conditions with food, and water ad libitum. Animals were assigned to HIIT or Non-trained groups. HIIT protocol was performed during six weeks. Speed was determined through the assesstment of the maximum oxygen consumption (VO 2max). HIIT consisted of short bouts (1 min) running on a treadmill at 10° inclination (85–100% of VO 2max) with 2 min of active recovery (60% of VO 2max , without inclination). Non-trained group was daily exposed to a disconnected treadmill for the same amount of time as HITT group. Both groups were submitted to the open field, and novel object recognition tasks after six weeks. Malondialdehyde concentration (MDA), superoxide dismutase (SOD) activity, and non-enzymatic antioxidant capacity (FRAP) were quantified to determine the redox state. HIIT presented increased levels of MDA, SOD, and FRAP (p < 0.05) in the cerebellar tissue, but no differences were seen in cerebral cortex. These results indicated an improved antioxidant capacity, despite increased MDA levels in the cerebellar tissue. Both groups did not present impairment in locomotor activity, development of anxious behavior or cognitive decline. HIIT enhanced the antioxidant defenses on cerebellar tissue with no deleterious effects on rats' cognition. [ABSTRACT FROM AUTHOR]

• Physical inactivity can contribute to worse epilepsy pathophysiology. • Physical exercise decreases the production of pro-inflammatory biomarkers. • Physical exercise reduces the number of epileptic seizures in epilepsy. • The regular practice of physical exercise enhances the levels of BDNF. • Physical exercise can be used as a non-pharmacological treatment in epilepsy. Epilepsy is a brain disorder that leads to seizures and neurobiological, cognitive, psychological, and social consequences. Physical inactivity can contribute to worse epilepsy pathophysiology. Here, we review how physical exercise affects epilepsy physiopathology. An extensive literature search was performed and the mechanisms of physical exercise on epilepsy were discussed. The search was conducted in Scopus and PubMed. Articles with relevant information were included. Only studies written in English were considered. The regular practice of physical exercise can be beneficial for individuals with neurodegenerative diseases, such as epilepsy by decreasing the production of pro-inflammatory and stress biomarkers, increasing socialization, and reducing the incidence of epileptic seizures. Physical exercise is also capable of reducing the symptoms of depression and anxiety in epilepsy. Physical exercise can also improve cognitive function in epilepsy. The regular practice of physical exercise enhances the levels of brain-derived neuro factor (BDNF) in the hippocampi, induces neurogenesis, inhibits oxidative stress and reactive gliosis, avoids cognitive impairment, and stimulates the production of dopamine in the epileptic brain. Physical exercise is an excellent non-pharmacological tool that can be used in the treatment of epilepsy. [ABSTRACT FROM AUTHOR]

It is known that a single session of high-intensity interval exercise (HIIE) contributes to the increase of the reactive species of oxygen, accompanied by a greater antioxidant activity. However, it is poorly understood if a single session of HIIE has similar effects on the brain tissue. This study evaluated the effects of a single HIIE on the hippocampal redox status. Sixteen males Wistar rats were allocated into HIIE (n = 8) and control (n = 8) groups. Maximum oxygen consumption (VO 2max) was evaluated using a treadmill at 10° inclination in a metabolic chamber. HIIE group was submitted to a single run on the treadmill composed by 10 bouts of high-intensity exercise of 1 min each (85–100% of VO 2max), at 28 m/min, 10° inclination, interspersed by 2 min of active recovery, at 10 m/min, with no inclination. Analysis of the redox status at the hippocampus were conducted 24 h after the HIIE session. It was not identified lipid peroxidation in the hippocampus of the HIIE group (Control 1.9 ± 0.31, vs HIIT 2.2 ± 0.53 nmol MDA/mg protein (p >.05). However, the activity of the superoxide dismutase (Control 2.614 ± 0.225 vs HIIT 3.718 ± 0.4589 U/mg protein), and the non-enzymatic total antioxidant capacity (Control 1584 ± 75.88 vs HIIT 1984 ± 137.7 nM FeSO4/mg protein) were enhanced (p <.05) after the exercise session. These results indicate that the antioxidant mechanisms are enhanced even after a single session of HIIE. A single session of HIIE does not induce lipid peroxidation and improves the antioxidant defenses in Wistar rats' hippocampus. • Antioxidant capacity is enhanced after a single session of high-intensity interval exercise (HIIE) on rats' hippocampus. • A single session of HIIE does not induce lipid peroxidation on rats' hippocampus. • A single session of HIIE improves enzymatic and non-enzymatic total antioxidant capacity in Wistar rats' hippocampus. [ABSTRACT FROM AUTHOR]