International Journal of Neuroscience Research


Review Article of International Journal of Neuroscience Research NEUROINFLAMMATION Gustavo Leite Franklin, M.D., Ph.D.1; Nayra de Souza Carvalho Lima, Msc.2; Alex Tiburtino Meira, M.D., Msc, Ph.D.3, Lucas Andrade Ferreti, M.D.1; Conrado Regis Borges, M.D4 1Universidade Federal do Paraná, Curitiba, Paraná. 2Universidade Vila Velha, Espírito Santo. 3 Universidade Federal da Paraíba, João Pessoa, Paraíba. 4Universidade de São Paulo – FMUSP, São Paulo 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 ...


Research Article of International Journal of Neuroscience Research Environmental Enrichment Reduces Cortical Excitability In Rats Submitted To Status Epilepticus In The Pilocarpine Model: An Evaluation From Cortical Spreading Depression Roberto Carlos da Silva Bandeira1, Luís Gustavo Carvalho dos Santos2, Christian Barker Silva Santisteban2, Angela Amancio-dos-Santos3 1Federal University of Pernambuco - UFPE, Health Sciences Center, Department of Pharmaceutical Sciences, Recife - PE, Brazil; 2Federal University of Pernambuco - UFPE, Medical Sciences Center, Recife - PE, Brazil; 3Federal University of Pernambuco - UFPE, Biosciences Center, Department of Physiology and Pharmacology, Recife - PE, Brazil 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. Keywords: epilepsy. cortical spreading depression. pilocarpine ...


Review Article of International Journal of Neuroscience Research The Impact of the Covid-19 Pandemic on the Mental Health of Health Professionals Maria Zilda Lacerda Assunção de Mello¹*, Alexia Venâncio Fideles¹, Raissa Lemos Fontes¹, Ramon Gonçalves de Melo Valente², Vitória Maria Gomes Rabelo¹, Héberte de Santana Arruda³. ¹Acadêmica de Medicina da Universidade Católica de Pernambuco, Recife.;²Acadêmico de Medicina da UNINASSAU, Recife.; ³Mestrando do Programa de Pós-Graduação em Dentística/Endodontia da Faculdade de Odontologia de Pernambuco. 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. Keywords: Mental health. Health professionals. Covid-19 ...


Review Article of International Journal of Neuroscience Research THE INFLUENCE OF MITOCHONDRIA IN ALZHEIMER DISEASE AND POSSIBLE ALTERNATIVE THERAPIES Ferro M1*, Graubard A1, Escalante P1, Channan G.1 1FG Scientifica and Science Department at Nutrition Formulators Inc., Miramar Florida 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 ...

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