Neurological consequences of exercise during prenatal Zika virus exposure to mice pups.

PURPOSE/AIM: 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. MATERIAL AND METHODS: 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. RESULTS: 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. CONCLUSION: Our findings reveal beneficial effects of exercise during pregnancy exposure to ZIKV in mice pups.

An update on potential links between type 2 diabetes mellitus and Alzheimer's disease.

Alzheimer's disease (AD) and type 2 diabetes (T2D) major feature is insulin resistance. Brain and peripheral insulin resistance lead to hyperglycemia, which contributes to the development of T2D-linked comorbidities, such as obesity and dyslipidemia. Individuals with hyperglycemia in AD present with neuronal loss, formation of plaques and tangles and reduced neurogenesis. Inflammation seems to play an essential role in the development of insulin resistance in AD and T2D. We conducted a literature review about the links between AD and T2D. Alterations in glucose metabolism result from changes in the expression of the insulin receptor substrates 1 and 2 (IRS-1 and IRS-2), and seem to be mediated by several inflammatory pathways being present in both pathologies. Although there are some similarities in the insulin resistance of AD and T2D, brain and peripheral insulin resistance also have their discrete features. Failure to activate IRS-1 is the hallmark of AD, while inhibition of IRS-2 is the main feature in T2D. Inflammation mediates the alterations in glucose metabolism in AD and T2D. Targeting inflammation and insulin receptors may be a successful strategy to prevent and ameliorate T2D and AD symptoms.

High-intensity resistance training induces changes in cognitive function, but not in locomotor activity or anxious behavior in rats induced to type 2 diabetes.

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 GSk3ß 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.

A single session of high-intensity interval exercise increases antioxidants defenses in the hippocampus of Wistar rats.

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 (VO2max) 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 VO2max), 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 ±â€¯0.31, vs HIIT 2.2 ±â€¯0.53 nmol MDA/mg protein (p > .05). However, the activity of the superoxide dismutase (Control 2.614 ±â€¯0.225 vs HIIT 3.718 ±â€¯0.4589 U/mg protein), and the non-enzymatic total antioxidant capacity (Control 1584 ±â€¯75.88 vs HIIT 1984 ±â€¯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.

High-intensity interval training improves cerebellar antioxidant capacity without affecting cognitive functions in rats.

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 (VO2max). HIIT consisted of short bouts (1 min) running on a treadmill at 10° inclination (85-100% of VO2max) with 2 min of active recovery (60% of VO2max, 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.