International Journal of Neuroscience Research
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Objective: To assess the impact on mental health of health professionals during the COVID-19 pandemic. Methods: Narrative review of the literature, of a descriptive character, carried out through bibliographic survey through a search strategy based on the terms: Mental health, Health professionals and Covid-19. Inclusion criteria were adopted: articles published in Portuguese, English and Spanish indexed in the PUBMED / MEDLINE, SciELO and VHL databases published between February 2020 and August 2020. Results: The COVID-19 pandemic established a chaos in all sectors of society, the health sphere was the most affected. The routine of health professionals was abruptly altered by the constant confrontation of an enormous pressure that goes from working in an environment with a high risk of contamination without adequate protection, excessive working hours, frustration, lack of contact with family to experiences of discrimination by a small part of society who see them as potential vectors of disease transmission. Conclusion: The pandemic was extremely harmful to the health of health professionals, affecting their emotional balance. It was shown that the pandemic scenario caused a lot of damage, as these professionals were exposed to high and intense workloads, which caused physical and mental exhaustion, leading to a feeling of weakness and professional insecurity.



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The epidemiology of Alzheimer’s disease (AD) is notable. North America and Western Europe have the most expressive rates of disease (6.4% and 5.4% at age 60), followed by Latin America (4.9%) and, finally China (4%). The most important fact is that head trauma increases the deposition of amyloid βeta (Aβ) and the expression of neuronal tau as well as diabetes. Obesityand trans fats also increase the risk of AD. However, virtually no current pharmacotherapy is approved for agitation / excitation caused by AD, the only purpose is maintaining the memory of those affected by this disease. There is substantial evidence that some dysfunctions in the mitochondria are involved in AD. Mitochondria are essential for neuronal function because the limited glycolytic metabolism of these cells makes them highly dependent on aerobic oxidative phosphorylation (OXPHOS) for their energy needs. Increased concentrations of ROS are known to result in molecular damage to the site where they are produced, triggering what science calls oxidative stress. Another no less important pathophysiological process in neurological disease is mitochondrial membrane cholesterol. New evidence indicates that the burden of mitochondrial cholesterol can influence mitochondrial function regardless of its conversion to pregnenolone or oxysterols, emerging as a key factor in the pathology of several neurological diseases associated with mitochondrial dysfunction, as in the case of AD. In this way, neurons are strictly dependent on the presence of healthy mitochondria, especially in the synapses where these organelles produce ATP and concentration of Ca2 + ions, fundamental processes for the implementation of neurotransmission and generation of membrane potential along the axon. Controlling ROS, as well as reducing the inflammatory cascade in neurons can be a good strategy in controlling the disease. The reduction of cholesterol in the external mitochondrial membrane may be another interesting path for the reentry of glutathione in the control of ROS, which occurs due to the imbalance in the metabolism of the mitochondrial respiratory chain seen in AD. In this review, we discuss the role of mitochondria in AD as well as alternative therapies for controlling this disease with specific herbal and nutraceuticals.



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OBJECTIVE: to verify the association between general health perceptions with a focus on sleep quality, eating activities and concentration areas of the course after university admission. METHOD: Cross-sectional study approved by ethics committee (n°2,581,563), with a sample of 432 undergraduate students from the Federal Public University, divided into three groups: Group 1: Humanities Students; Group 2: Health Students; Group 3: Exact Science students. For the collection, we used: vivências Acadêmicas’s questionnaire in the reduced version, and a sociodemographic questionnaire. Descriptive and inferential statistical techniques were used for analysis, considering a significance level of 5%. RESULTS: In the general sample, all general health perceptions were impaired after entering the University. In the analysis of the groups, it is noticed that Group 1 presented more negative rates of health perception (47.3% p (1) = 0.016), with significant and significant sleep-related impairments (68.2% p (1) = 0.002). On the other hand, the students in Group 3 presented the worst perceptions about the quality of food and difficulties in performing leisure activities (p (1) = 0.005). CONCLUSION: There was a significant association between university admission and negative health perceptions. In addition, it was found that the students in the humanities and exact areas were the most vulnerable. Thus, it can be considered that academic experience can contribute negatively to the promotion of the health of young people, and, in this sense, it is recommended the implementation of educational programs aimed at self-care, prevention of academic stress and its negative effects on health.



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Objective: This study verified if the exposure to environmental enrichment (EE) influences brain excitability, evaluated by cortical spreading depression (CSD), in rats submitted to status epilepticus (SE). Methods: At 35 days of age, male Wistar rats were divided into two experimental groups: pilocarpine (PILO), which received a single dose of pilocarpine hydrochloride to induce SE, and saline (SAL), which were the group control. On the following day, half of the animals in each group were exposed to EE; while the other half was kept in the standard environment (S), considered control. At 67 days of age, the rats were anesthetized and submitted to CSD. Results: Pilocarpine, isolated, reduced the speed of propagation and increased the duration and amplitude of CSD. EE, itself, reduced the speed of propagation and duration, but increased the amplitude of CSD. In the animals exposed to EE that undergone SE, the values of CSD parameters became closer to the control group. Conclusion: Our results indicate that EE reduced the cortical excitability induced by SE, possibly by promoting antioxidant effects at the brain level, inducing neurogenesis and/or improving the excitatory/inhibitory balance of neurotransmitters.



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Inflammation is a complex process, mediated by cellular and molecular mechanisms caused by a response to a tissue damage from an aggressive agent, whether if biological, chemical or physical origin. This process occurs, ultimately, with the purpose of promoting defense, repair and tissue regeneration. The inflammatory process leads to changes in blood vessels that have their diameter and flow altered, with the objective of leading to increased vascular permeability and consequent leakage of fluids and cells into the extracellular space of the affected tissue. This sequence of events generates the cardinal signs of inflammation, which are: pain, heat, redness, edema, with loss or alteration of function. The process occurs through mechanisms induced by cytokines and that despite having local manifestation, it can lead to systemic responses involving the whole organism with fever, chills, tremors, tachycardia, leukocytosis, sweating, diuresis and blood dyscrasias. In the cascade of events related to inflammation, there is initially a local stimulus that promotes morphological and functional changes in the attacked tissue that trigger the release of signaling molecules, the defensins that have a chemotactic effect on monocytes, neutrophils and lymphocytes, and pro-inflammatory mediators. that are directly involved in the next inflammatory phases. There is, then, the recognition of aggression and the aggressor agent by the receptors of cells of the immune system and release of inflammatory mediators, of the cyclooxygenase pathway that will release prostaglandin, prostacyclins and thromboxanes and by the lipooxygenase pathway that will produce leukotrienes (Figure 1). Then, there is a modification of the local microcirculation promoting vasodilation, initially arteriolar and subsequently of the venules by the action of histamine release by mast cells, and associated with an increase in local blood flow, generate the cardinal flushing and heat signals.



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