The neurobiological effects of senescence on dopaminergic system: A comprehensive review.

Over time, the body undergoes a natural, multifactorial, and ongoing process named senescence, which induces changes at the molecular, cellular, and micro-anatomical levels in many body systems. The brain, being a highly complex organ, is particularly affected by this process, potentially impairing its numerous functions. The brain relies on chemical messengers known as neurotransmitters to function properly, with dopamine being one of the most crucial. This catecholamine is responsible for a broad range of critical roles in the central nervous system, including movement, learning, cognition, motivation, emotion, reward, hormonal release, memory consolidation, visual performance, sexual drive, modulation of circadian rhythms, and brain development. In the present review, we thoroughly examine the impact of senescence on the dopaminergic system, with a primary focus on the classic delimitations of the dopaminergic nuclei from A8 to A17. We provide in-depth information about their anatomy and function, particularly addressing how senescence affects each of these nuclei.

Adult human neural cells in culture following traumatic brain injury

Objective: The present study aims to evaluate the viability of adult human neural cells in culture obtained from traumatized brain tissues collected in emergency surgery procedures. Methods: Exploratory, descriptive, quantitative and cross-sectional study evaluating samples obtained from patients who underwent traumatic brain injury with extrusion of brain tissue submitted to cell culture in a standardized medium, being preserved during 168h. After observation under phase contrast microscopy and immunohistochemical processing for neuronal (MAP-2) and glial (GFAP) markers, morphometric parameters of neural cells (cell body area, dendritic field length and fractal dimension) were evaluated using ImageJ software, with data obtained after 24, 72 and 168h being compared using non-parametric Kruskal Wallis test, followed by Dunn's post hoc test. Results: The explant of the nervous tissue revealed a consolidated pattern of cell migration into the culture medium. Cell proliferation, upon reaching confluence, presented an aspect of cellular distribution juxtaposed along the culture medium at all time points analyzed. Both neurons and glial cells remained viable after 168h in culture, with their morphologies not varying significantly throughout the time points evaluated. Immunohistochemistry for MAP-2 showed a relatively well-preserved cytoskeletal organization. GFAP immunoreactivity revealed activated astrocytes especially at the later time point. Conclusions: Our results point out the viability of cell culture from traumatized human nervous tissue, opening up perspectives for the use of substances of natural origin that may contribute neuroprotectively to neuronal maintenance in culture, allowing future translational approach.

Fatores de risco para a Síndrome de burnout em enfermeiros de um hospital público de Mossoró/RN, Brasil / Risk factors for burnout syndrome in nurses at a public hospital in Mossoró/RN, Brazil

Objetivo: Avaliar os fatores de risco para o aparecimento da Síndrome de burnout em enfermeiros trabalhadores do Hospital Regional Tarcísio de Vasconcelos Maia em Mossoró/RN. Métodos: Estudo exploratório, descritivo, quantitativo e transversal com 119 enfermeiros de março a setembro de 2022. Os dados foram coletados a partir da aplicação de um formulário com informações sócio-organizacionais e do Copenhagen Burnout Inventory, contendo 19 itens que refletem o burnout profissional em uma escala categorizada como burnout baixo, intermediário e alto. Resultados: A maioria dos entrevistados era do sexo feminino (81%), com média de 36,4 anos de idade, casada (70%), com especialização na área (74%) e dois empregos (59%). Identificou-se maior prevalência de níveis elevados de burnout pessoal (44%) e níveis intermediários de burnoutrelacionado ao trabalho (52%) e relacionado ao cliente (50%). Houve forte correlação positiva entre número de vínculos empregatícios para as dimensões burnout pessoal (r = 0,74; p = 0,03) e relacionado ao trabalho (r = 0,81; p = 0,02), forte correlação positiva entre carga horária de trabalho e burnout pessoal (r = 0,68; p = 0,04) e moderada correlação positiva entre carga horária de trabalho e burnout relacionado ao trabalho (r = 0,53; p = 0,04). Conclusões: A exposição a jornadas de trabalho prolongadas resultou em aumento dos níveis de exaustão física e psíquica nos enfermeiros, interferindo negativamente nos aspectos profissionais e pessoais. Estudos futuros focando em estratégias para garantir uma melhor condição de trabalho ao enfermeiro são necessários, visando proporcionar uma melhor saúde ocupacional aos trabalhadores

Objective: To evaluate the risk factors for the onset of burnout syndrome in nursing workers at the Hospital Regional Tarcísio de Vasconcelos Maia in Mossoró/RN. Methods: Exploratory, descriptive, quantitative and cross-sectional study with 119 nurses from March to September 2022. Data were collected from the application of a form with socio-organizational information and the Copenhagen Burnout Inventory, containing 19 items that reflect the professional burnout on a scale categorized as low, intermediate and high burnout. Results: Most respondents were female (81%), with an average age of 36.4 years, married (70%), with specialization in the area (74%) and two jobs (59%). A higher prevalence of high levels of personal burnout (44%) and intermediate levels of work-related (52%) and client-related burnout (50%) were identified. There was a strong positive correlation between the number of employment relationships for the personal burnout (r = 0.74; p = 0.03) and work-related (r = 0.81; p = 0.02) dimensions, a strong positive correlation between load hours of work and personal burnout (r = 0.68; p = 0.04) and a moderate positive correlation between workload and work-related burnout (r = 0.53; p = 0.04). Conclusions: Exposure to long working hours resulted in increased levels of physical and mental exhaustion in nurses, negatively interfering with professional and personal aspects. Future studies focusing on strategies to ensure a better working condition for nurses are needed, aiming to provide better occupational health for workers. Keywords: Burnout syndrome; Occupational stress; Nursing

Avaliação da comunicação social de crianças até 12 anos com Transtorno do Espectro Autista em Centro de Atendimento Psicossocial / Evaluation of the social communication of children up to 12 years old with Autism Spectrum Disorder in a Psychosocial Care Center

Objetivo: Caracterizar a comunicação social em crianças até 12 anos diagnosticadas com Transtorno do Espectro Autista (TEA) atendidos no Centro de Atenção Psicossocial Infantil (CAPSi) da cidade de Mossoró/RN. Métodos: Pesquisa exploratória, descritiva, quantitativa, transversal, realizada no CAPSi de Mossoró/RN. A coleta de dados baseou-se na aplicação de questionários aos pais/responsáveis, para caracterizar suas condições socioeconômicas e sua percepção sobre seus filhos. Foi utilizado o instrumento Avaliação do Desenvolvimento da Linguagem (ADL) para crianças, desenvolvido para avaliar a aquisição e desenvolvimento de conteúdo (semântica) e estrutura (morfologia e sintaxe) da linguagem. Os questionários foram codificados e os dados foram tabulados para posterior análise estatística. Resultados: Foram estudadas 33 crianças e 73 pais/responsáveis. A maioria dos pais/responsáveis era do sexo feminino (95,9%), predominantemente na faixa etária de 30-39 anos (média de 37,6 anos), com cônjuge (60%), com ensino médio completo (45%) e renda mensal em torno de um salário-mínimo (76,7%), possuindo atitudes positivas em relação aos filhos e notando dificuldades na comunicação destes. Na aplicação do questionário com as crianças, 63,7% apresentaram resultados na faixa de normalidade, enquanto 3% apresentaram alteração leve e 33,3% alteração grave de linguagem. Conclusão: Crianças com TEA frequentadoras do CAPSi apresentam alterações de linguagem no subnível pragmático e mais da metade dos participantes não apresenta alterações morfossintáticas e semânticas

Objective: To characterize social communication in children up to 12 years old diagnosed with Autistic Spectrum Disorder (ASD) treated at the Child Psychosocial Care Center (CAPSi) in Mossoró/RN. Methods: Exploratory, descriptive, quantitative, cross-sectional study conducted at CAPSi in Mossoró/RN. The data collection was based on the application of questionnaires to parents/guardians to characterize their socioeconomic conditions and their perception of their children. The Language Development Assessment (LDA) instrument for children was used, developed to assess the acquisition and development of language content (semantics) and structure (morphology and syntax). The questionnaires were coded, and the data were tabulated for further statistical analysis. Results: 33 children and 73 parents/guardians were studied. Most parents/guardians were female (95.9%), aged 30-39 years (mean age 37.6 years predominantly), with a partner (60%), with high school education (45%), and monthly income around one minimum wage (76.7%), having positive attitudes toward their children and noticing difficulties in their communication. In applying the questionnaire to the children, 63.7% presented results within the normal range, while 3% presented mild and 33.3% severe language alterations. Conclusion: Children with ASD attending CAPSi have language disorders in the pragmatic sublevel, and more than half of the participants did not have morphosyntactic and semantic changes

Cellular and Molecular Pathophysiology of Traumatic Brain Injury: What Have We Learned So Far?

Traumatic brain injury (TBI) is one of the leading causes of long-lasting morbidity and mortality worldwide, being a devastating condition related to the impairment of the nervous system after an external traumatic event resulting in transitory or permanent functional disability, with a significant burden to the healthcare system. Harmful events underlying TBI can be classified into two sequential stages, primary and secondary, which are both associated with breakdown of the tissue homeostasis due to impairment of the blood-brain barrier, osmotic imbalance, inflammatory processes, oxidative stress, excitotoxicity, and apoptotic cell death, ultimately resulting in a loss of tissue functionality. The present study provides an updated review concerning the roles of brain edema, inflammation, excitotoxicity, and oxidative stress on brain changes resulting from a TBI. The proper characterization of the phenomena resulting from TBI can contribute to the improvement of care, rehabilitation and quality of life of the affected people.

Aerobic Physical Training Attenuates Oxidative Stress in the Spinal Cord of Adult Rats Induced by Binge-like Ethanol Intake.

Binge drinking is the most frequent consumption pattern among young adults and remarkably changes the central nervous system; thus, research on strategies to protect it is relevant. This study aimed to investigate the detrimental effects of binge-like EtOH intake on the spinal cord of male rats and the potential neuroprotective effects provided by moderate-intensity aerobic physical training. Male Wistar rats were distributed into the 'control group', 'training group', 'EtOH group', and 'training + EtOH'. The physical training protocol consisted of daily 30-min exercise on a treadmill for 5 consecutive days followed by 2 days off during 4 weeks. After the fifth day of each week, distilled water ('control group' and 'training group') or 3 g/kg of EtOH diluted at 20% w/v ('EtOH group' and 'training + EtOH group') was administered for 3 consecutive days through intragastric gavage to simulate compulsive consumption. Spinal cord samples were collected for oxidative biochemistry and morphometric analyses. The binge-like EtOH intake induced oxidative and tissue damage by decreasing reduced glutathione (GSH) levels, increasing lipid peroxidation (LPO), and reducing motor neurons (MN) density in the cervical segment. Even under EtOH exposure, physical training maintained GSH levels, reduced LPO, and prevented MN reduction at the cervical segment. Physical training is a non-pharmacological strategy to neuroprotect the spinal cord against oxidative damage induced by binge-like EtOH intake.

Astrocytosis, Inflammation, Axonal Damage and Myelin Impairment in the Internal Capsule following Striatal Ischemic Injury.

Secondary degeneration is defined as a set of destructive events that damage cells and structures that were initially spared or only peripherally affected by the primary insult, constituting a key factor for functional impairment after traumatic brain injury or stroke. In the present study, we evaluated the patterns of astrocytosis, inflammatory response, axonal damage and oligodendrocytes/myelin impairment in the internal capsule following a focal injection of endothelin-1 (ET-1) into the dorsal striatum. Animals were perfused at 1, 3 and 7 post-lesion days (PLD), and tissue was processed to immunohistochemistry for neutrophils (MBS1), macrophages/microglia (ED1), astrocytes (GFAP), axonal lesion (ßAPP), oligodendrocytes (Tau) and myelin (MBP). A significant number of neutrophils was observed at 1PLD, followed by intense recruitment/activation of macrophages/microglia at 3PLD and astrocytic reaction with a peak at 7PLD. Oligodendrocyte damage was pronounced at 3PLD, remaining at 7PLD. Progressive myelin impairment was observed, with reduction of immunoreactivity at 7PLD. Axonal lesion was also identified, mainly at 7PLD. Our results indicate that acute inflammatory response elicited by the ischemic insult in the striatum can be associated with the axonal impairment and damage of both oligodendrocytes and myelin sheath identified in the internal capsule, which may be related to loss of tissue functionality observed in secondary degeneration.

Organization of Somatosensory Cortex in the South American Rodent Paca (Cuniculus paca).

INTRODUCTION: The study of non-laboratory species has been part of a broader effort to establish the basic organization of the mammalian neocortex, as these species may provide unique insights relevant to cortical organization, function, and evolution. METHODS: In the present study, the organization of three somatosensory cortical areas of the medium-sized (5-11 kg body mass) Amazonian rodent, the paca (Cuniculus paca), was determined using a combination of electrophysiological microelectrode mapping and histochemical techniques (cytochrome oxidase and NADPH diaphorase) in tangential sections. RESULTS: Electrophysiological mapping revealed a somatotopically organized primary somatosensory cortical area (S1) located in the rostral parietal cortex with a characteristic foot-medial/head-lateral contralateral body surface representation similar to that found in other species. S1 was bordered laterally by two regions housing neurons responsive to tactile stimuli, presumably the secondary somatosensory (S2) and parietal ventral (PV) cortical areas that evinced a mirror-reversal representation (relative to S1) of the contralateral body surface. The limits of the putative primary visual (V1) and primary auditory (A1) cortical areas, as well as the complete representation of the contralateral body surface in S1, were determined indirectly by the histochemical stains. Like the barrel field described in small rodents, we identified a modular arrangement located in the face representation of S1. CONCLUSIONS: The relative location, somatotopic organization, and pattern of neuropil histochemical reactivity in the three paca somatosensory cortical areas investigated are similar to those described in other mammalian species, providing additional evidence of a common plan of organization for the somatosensory cortex in the rostral parietal cortex of mammals.

Global Proteomic Profile of Aluminum-Induced Hippocampal Impairments in Rats: Are Low Doses of Aluminum Really Safe?

Hippocampus is the brain area where aluminum (Al) accumulates in abundance and is widely associated with learning and memory. In the present study, we evaluate behavioral, tissue, and proteomic changes in the hippocampus of Wistar rats caused by exposure to doses that mimic human consumption of aluminum chloride (AlCl3) in urban areas. For this, male Wistar rats were divided into two groups: Control (distilled water) and AlCl3 (8.3 mg/kg/day), both groups were exposed orally for 60 days. After the Al exposure protocol, cognitive functions were assessed by the Water maze test, followed by a collection for analysis of the global proteomic profile of the hippocampus by mass spectrometry. Aside from proteomic analysis, we performed a histological analysis of the hippocampus, to the determination of cell body density by cresyl violet staining in Cornu Ammonis fields (CA) 1 and 3, and hilus regions. Our results indicated that exposure to low doses of aluminum chloride triggered a decreased cognitive performance in learning and memory, being associated with the deregulation of proteins expression, mainly those related to the regulation of the cytoskeleton, cellular metabolism, mitochondrial activity, redox regulation, nervous system regulation, and synaptic signaling, reduced cell body density in CA1, CA3, and hilus.

Intrauterine and Postnatal Exposure to High Levels of Fluoride Is Associated with Motor Impairments, Oxidative Stress, and Morphological Damage in the Cerebellum of Offspring Rats.

Fluoride (F) is abundantly present on Earth and plays a beneficial role in human health. However, exposure to high doses of F can be a risk, mainly in endemic fluorosis regions. In light of this, we investigated the effects of F exposure during the intrauterine and postnatal periods of rats, in doses similar to those recommended in drinking water and the levels of F in regions with endemic fluorosis, on the offspring rats' cerebellum. Pregnant rats were divided into three groups: control (received ultrapure water only), 10 mg F/L, and 50 mg F/L for a period of 42 days (21 days gestation and 21 days lactation). At the end of the lactation period, the male pups were evaluated by behavioral tests, morphological markers, and biochemistry assays. The results pointed out that 50 mg F/L exposure during the intrauterine and lactational period of rats is capable of promoting oxidative stress in the cerebellum with a decrease in Purkinje cell density and myelin basic protein compromise, which could be associated with functional motor impairments. In addition, although 10 mg F/L exposure promoted redox alterations, it did not affect other parameters evaluated, highlighting the safe use of F in low doses.

Microelectrode implants, inflammatory response and long-lasting effects on NADPH diaphorase neurons in the rat frontal cortex.

At present, one of the main therapeutic challenges comprises the development of technologies to improve the life quality of people suffering from different types of body paralysis, through the reestablishment of sensory and motor functions. In this regard, brain-machine interfaces (BMI) offer hope to effectively mitigate body paralysis through the control of paralyzed body parts by brain activity. Invasive BMI use chronic multielectrode implants to record neural activity directly from the brain tissue. While such invasive devices provide the highest amount of usable neural activity for BMI control, they also involve direct damage to the nervous tissue. In the cerebral cortex, high levels of the enzyme NADPH diaphorase (NADPH-d) characterize a particular class of interneurons that regulates neuronal excitability and blood supply. To gain insight into the biocompatibility of invasive BMI, we assessed the impact of chronic implanted tungsten multielectrode bundles on the distribution and morphology of NADPH-d-reactive neurons in the rat frontal cortex. NADPH-d neuronal labeling was correlated with glial response markers and with indices of healthy neuronal activity measured by electrophysiological recordings performed up to 3 months after multielectrode implantation. Chronic electrode arrays caused a small and quite localized structural disturbance on the implanted site, with neuronal loss and glial activation circumscribed to the site of implant. Electrodes remained viable during the entire period of implantation. Moreover, neither the distribution nor the morphology of NADPH-d neurons was altered. Overall, our findings provide additional evidence that tungsten multielectrodes can be employed as a viable element for long-lasting therapeutic BMI applications.

Effect of senescence on the tyrosine hydroxylase and S100B immunoreactivity in the nigrostriatal pathway of the rat.

Senescence is a natural and progressive physiological event that leads to a series of morphophysiological alterations in the organism. The brain is the most vulnerable organ to both structural and functional changes during this process. Dopamine is a key neurotransmitter for the proper functioning of the brain, directly involved in circuitries related with emotions, learning, motivation and reward. One of the main dopamine- producing nuclei is the substantia nigra pars compacta (SNpc), which establish connections with the striatum forming the so-called nigrostriatal pathway. S100B is a calcium binding protein mainly expressed by astrocytes, involved in both intracellular and extracellular processes, and whose expression is increased following injury in the nervous tissue, being a useful marker in altered status of central nervous system. The present study aimed to analyze the impact of senescence on the cells immunoreactive for tyrosine hydroxylase (TH) and S100B along the nigrostriatal pathway of the rat. Our results show an decreased expression of S100B+ cells in SNpc. In addition, there was a significant decrease in TH immunoreactivity in both projection fibers and TH+ cell bodies. In the striatum, a decrease in TH immunoreactivity was also observed, as well as an enlargement of the white matter bundles. Our findings point out that senescence is related to the anatomical and neurochemical changes observed throughout the nigrostriatal pathway.

Methylmercury Causes Neurodegeneration and Downregulation of Myelin Basic Protein in the Spinal Cord of Offspring Rats after Maternal Exposure.

Methylmercury (MeHg) is one of the most dangerous toxic pollutants spread throughout the earth. Chronic MeHg intoxication by contaminated food ingestion is the most common threat to human health, including impairment to the developing fetus. The present study aims at investigating the effects of maternal exposure to MeHg during gestation and lactation on the spinal cord of offspring. Pregnant rats received oral doses of MeHg (40 µg/kg/day) over a period of 42 days (21 gestation and 21 lactation). Control animals received the vehicle only. Total mercury concentration was measured in blood samples from offspring collected at the 41st postnatal day. Counting of motor neurons and immunoreactivity for myelin basic protein (MBP) were assessed in the spinal cords in both control and MeHg-intoxicated animals. Our results showed that MeHg promoted an increase in blood Hg levels. In addition, it caused a reduction in the number of spinal cord motor neurons as well as decreased MBP immunoreactivity in the cervical, thoracic and lumbar segments. Our present findings suggest that MeHg intoxication during rat pregnancy and lactation is associated with a pattern of motor neuron degeneration and downregulation of myelin basic protein in different segments of a developing spinal cord. Further studies are needed to establish the effect of MeHg intoxication in both young and adult rats.

Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study.

The environmental contamination by methylmercury (MeHg) is a major concern for public health. The effects of MeHg in the central nervous system (CNS) of adult animals have been extensively investigated; however, little is known about the effects of MeHg exposure during intrauterine and lactation periods on motor and cognitive functions of adolescent rats. Therefore, this study aimed to investigate the effect of MeHg exposure during intrauterine life and lactation on both motor and cognitive functions of offspring rats. Ten female Wistar rats were exposed to 40 µg/kg/day of MeHg through cookie treats from the first day of pregnancy until the last day of breastfeeding. Both motor and cognitive functions of offspring male rats were assessed by open field, rotarod, and step-down inhibitory avoidance tests. Forty-one days after birth, the hippocampus and cerebellum were collected to determine total Hg content, antioxidant capacity against peroxyl radicals (ACAP), reduced glutathione (GSH) levels, lipid peroxidation (LPO), and nitrite levels. MeHg exposure during CNS development increased Hg levels in both hippocampal and cerebellar parenchymas, triggered oxidative stress throughout ACAP and GSH decrease, increased LPO and nitrite levels. These alterations resulted in reduced spontaneous and stimulated locomotion and short- and long-term memory deficits. Therefore, damages triggered by MeHg exposure during intrauterine life and lactation had detrimental effects on oxidative biochemistry and motor and cognitive functions of offspring rats.

Inflammatory Response and Secondary White Matter Damage to the Corpus Callosum after Focal Striatal Stroke in Rats.

Stroke is one of the leading causes of death and long-term disabilities worldwide, resulting in a debilitating condition occasioned by disturbances in the cerebral vasculature. Primary damage due to metabolic collapse is a quick outcome following stroke, but a multitude of secondary events, including excitotoxicity, inflammatory response, and oxidative stress cause further cell death and functional impairment. In the present work, we investigated whether a primary ischemic damage into the dorsal striatum may cause secondary damage in the circumjacent corpus callosum (CC). Animals were injected with endothelin-1 and perfused at 3, 7, 14, and 30 post-lesion days (PLD). Sections were stained with Cresyl violet for basic histopathology and immunolabeled by antibodies against astrocytes (anti-GFAP), macrophages/microglia (anti-IBA1/anti MHC-II), oligodendrocytes (anti-TAU) and myelin (anti-MBP), and Anti-Nogo. There were conspicuous microgliosis and astrocytosis in the CC, followed by later oligodendrocyte death and myelin impairment. Our results suggest that secondary white matter damage in the CC follows a primary focal striatal ischemia in adult rats.

Motor, memory, and anxiety-like behavioral impairments associated with brain-derived neurotrophic factor and dopaminergic imbalance after inhalational exposure to deltamethrin.

Believed to cause damage to the nervous system and possibly being associated with neurodegenerative diseases, deltamethrin (DM) is a type II pyrethroid used in pest control, public health, home environment, and vector control. The objective of this study was to evaluate the motor, cognitive and emotional changes associated with dopaminergic and BDNF imbalance after DM exposure in rats. Sixty Wistar rats (9-10 months-old) were used, under Ethics Committee on Animal Research license (ID 19/2017). The animals were randomly divided into four groups: control (CTL, 0.9% saline), DM2 (2 mg DM in 1.6 mL 0.9% saline), DM4 (4 mg of DM in 1.6 mL of 0.9% saline), and DM8 (8 mg of DM in 1.6 mL of 0.9% saline). DM groups were submitted to 9 or 15 inhalations, one every 48 h. Half of the animals from each group were randomly selected and perfused 24 h after the 9th or 15th inhalation. Throughout the experiment, the animal's behavior were evaluated using catalepsy test, open field, hole-board test, Modified Elevated Plus Maze, and social interaction. At the end of the experiments, the rats were perfused transcardially and their brains were processed for Tyrosine Hydroxylase (TH) and Brain derived neurotrophic factor (BDNF) immunohistochemistries. The animals submitted to 9 inhalations of DM showed a reduction in immunoreactivity for TH in the Substantia nigra pars compacta (SNpc), ventral tegmental area (VTA), and dorsal striatum (DS) areas, and an increase in BDNF in the DS and CA1, CA3 and dentate gyrus (DG) hippocampal areas. Conversely, the animals submitted to 15 inhalations of DM showed immunoreactivity reduced for TH in the SNpc and VTA, and an increase in BDNF in the hippocampal areas (CA3 and DG). Our results indicate that the DM inhalation at different periods induce motor and cognitive impairments in rats. Such alterations were accompanied by dopaminergic system damage and a possible dysfunction on synaptic plasticity.

S100B protein: general characteristics and pathophysiological implications in the Central Nervous System.

BACKGROUND: Calcium-binding proteins are heterogeneous proteins that act binding this ion in specific domains, performing numerous functions. OBJECTIVE: In the present review, we aim to gather principal information about S100B protein in the Central Nervous System (CNS), highlighting its particularities, mapping, functionalities, and consequences on CNS dysfunction. METHODS: The research was carried out by searching Pubmed, Medline, Science Direct, Lilacs, the Cochrane Library, and Web of Science databases using the following descriptors: S100 protein; Central Nervous System; Nervous Lesions, as well as their corresponding terms in Portuguese and Spanish. The terms were first searched separately, then together. RESULTS: Due to its ability to bind with calcium, S100B is involved in the regulation of several intra- and extracellular physiological processes. As well as being multifunctional, this protein can be considered both a "marker" and "signaling" since it is capable of triggering functions of detection of and protection in situations of injury to the CNS. CONCLUSIONS: In-depth studies are necessary to discover the innumerable actions of this protein which are still unknown. It is expected that these can bring varied benefits by elucidating its therapeutic potential in preclinical and clinical situations.

Lead-Induced Motor Dysfunction Is Associated with Oxidative Stress, Proteome Modulation, and Neurodegeneration in Motor Cortex of Rats.

Lead (Pb) is a toxic metal with great neurotoxic potential. The aim of this study was to investigate the effects of a long-term Pb intoxication on the global proteomic profile, oxidative biochemistry and neuronal density in motor cortex of adult rats, and the possible outcomes related to motor functions. For this, Wistar rats received for 55 days a dose of 50 mg/Kg of Pb acetate by intragastric gavage. Then, the motor abilities were evaluated by open field and inclined plane tests. To investigate the possible oxidative biochemistry modulation, the levels of pro-oxidant parameters as lipid peroxidation and nitrites were evaluated. The global proteomic profile was evaluated by ultraefficiency liquid chromatography system coupled with mass spectrometry (UPLC/MS) followed by bioinformatic analysis. Moreover, it was evaluated the mature neuron density by anti-NeuN immunostaining. The statistical analysis was performed through Student's t-test, considering p < 0.05. We observed oxidative stress triggering by the increase in malonaldehyde and nitrite levels in motor cortex. In the proteomic analysis, the motor cortex presented alterations in proteins associated with neural functioning, morphological organization, and neurodegenerative features. In addition, it was observed a decrease in the number of mature neurons. These findings, associated with previous evidences observed in spinal cord, cerebellum, and hippocampus under the same Pb administration protocol, corroborate with the motor deficits in the rats towards Pb. Thus, we conclude that the long-term administration to Pb in young Wistar rats triggers impairments at several organizational levels, such as biochemical and morphological, which resulted in poor motor performance.

Essential Oils in Experimental Models of Neuropsychiatric Disorders: A Systematic Review.

BACKGROUND: Neural cells undergo functional or sensory loss due to neurological disorders. In addition to environmental or genetic factors, oxidative stress is a major contributor to neurodegeneration. In this context, there has been a growing interest in investigating the effects of EOs (EOs) in recent years, especially in the treatment of neuropathologies. The chemical and biological effects of EOs have led to important treatment tools for the management of various neurological disorders. OBJECTIVE: In the present study we performed a systematic review that sought to comprehend the neuroprotective effects of different EOs. METHOD: This work is a systematic review where an electronic search was performed on PubMed, ScienceDirect, Cochrane Library and SciELO (Scientific Electronic Library Online) databases, covering the last 10 years, using "Essential oil" and "Neuroprotective effect" as reference terms. RESULTS: A total of 9 articles were identified, in which the efficacy of EOs was described in experimental models of anxiety, dementia, oxidative stress, cerebral ischemia, Alzheimer's disease, and oxidative toxicity. CONCLUSION: EOs from different species of medicinal plants have shown positive responses in neurological disorders such as anxiety, dementia, oxidative stress, cerebral ischemia, and oxidative toxicity. Thus, EOs emerges with the potential to be used as alternative agents in the treatment of neurological disorders.

Association between Tooth Loss and Stroke: A Systematic Review.

This systematic review aims to evaluate the association between tooth loss and stroke. The Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) guidelines were followed. The PECO strategy was used to limit the eligibility criteria. The following databases were used on searches: PubMed, Scopus, Web of Science, The Cochrane Library, LILACS and OpenGrey. We included observational studies performed in adults (Population), in which patients with tooth loss (Exposition) and patients without tooth loss (Comparison) were observed to investigate the association between tooth loss and stroke (Outcome). After searches, the results were submitted to a selection process, followed by data extraction, quality assessment and risk of bias evaluation. The certainty of the evidence was evaluated through GRADE approach. A total of 925 potential studies were retrieved by the searches and 9 were included in this review. Seven of the included articles described an association between tooth loss and stroke. Low risk of bias and a low certainty of the evidence were identified to all studies. The certainty of the evidence may be associated with the observational nature of the included studies. Even though an association between tooth loss and stroke was suggested, the low strength of the current evidence indicated the need for further investigations with a better methodological design to conclude this question.