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Coronavirus disease 2019 (COVID-19) has been linked to various neurological complications. This meta-analysis assessed the relationship between glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) levels in the blood and neurological injury in COVID-19 patients. A comprehensive search of various databases was conducted until 18 August 2023, to find studies reporting GFAP and NfL blood levels in COVID-19 patients with neurological complications. GFAP and NfL levels were estimated between COVID-19 patients and healthy controls, and meta-analyses were performed using RevMan 5.4 software for analysis. In the 21 collected studies, it was found that COVID-19 patients had significantly higher levels of pooled GFAP (SMD = 0.52; 95% CI: 0.31, 0.73; p ≤ 0.001) and NfL (SMD = 0.60; 95% CI: 0.37, 0.82; p ≤ 0.001) when compared to the healthy controls. The pooled GFAP (SMD = 0.86; 95% CI: 0.26, 1.45; p ≤ 0.01) and NfL (SMD = 0.87; 95% CI: 0.48, 1.26; p ≤ 0.001) were significantly higher in non-survivors. These findings indicate a significant association between COVID-19 severity and elevated levels of GFAP and NfL, suggesting that GFAP and NfL could serve as potential diagnostic and prognostic markers for the early detection and monitoring of COVID-19-related neurological injuries.
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COVID-19 , Humanos , Prognóstico , COVID-19/complicações , Biomarcadores , Proteína Glial Fibrilar Ácida , Proteínas de Neurofilamentos , Filamentos Intermediários/metabolismoRESUMO
Neurogenesis is the process by which functional new neurons are generated from the neural stem cells (NSCs) or neural progenitor cells (NPCs). Increasing lines of evidence show that neurogenesis impairment is involved in different neurological illnesses, including mood disorders, neurogenerative diseases, and central nervous system (CNS) injuries. Since reversing neurogenesis impairment was found to improve neurological outcomes in the pathological conditions, it is speculated that modulating neurogenesis is a potential therapeutic strategy for neurological diseases. Among different modulators of neurogenesis, melatonin is a particularly interesting one. In traditional understanding, melatonin controls the circadian rhythm and sleep-wake cycle, although it is not directly involved in the proliferation and survival of neurons. In the last decade, it was reported that melatonin plays an important role in the regulation of neurogenesis, and thus it may be a potential treatment for neurogenesis-related disorders. The present review aims to summarize and discuss the recent findings regarding the protective effects of melatonin on the neurogenesis impairment in different neurological conditions. We also address the molecular mechanisms involved in the actions of melatonin in neurogenesis modulation.
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Melatonina/uso terapêutico , Doenças do Sistema Nervoso/tratamento farmacológico , Doenças do Sistema Nervoso/genética , Neurogênese , Substâncias Protetoras/uso terapêutico , Envelhecimento/patologia , Animais , Humanos , Melatonina/farmacologia , Neurogênese/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Substâncias Protetoras/farmacologiaRESUMO
Abuse of cough mixture is increasingly prevalent worldwide. Clinical studies showed that chronic consumption of cough mixture at high dosages may lead to psychiatric symptoms, especially affective disturbances, with the underlying mechanisms remain elusive. The present study aims at exploring the effect of repeated, high-dose dextromethorphan (DXM, a common active component of cough mixture) treatment on adult hippocampal neurogenesis, which is associated with pathophysiology of mood disturbances. After treatment with a high-dose of DXM (40 mg/kg/day) for 2 weeks, Sprague-Dawley rats showed increased depression-like behavior when compared to the control animals. Neurogenesis in the hippocampus was suppressed by DXM treatment, which was indicated by decreases in number of proliferative cells and doublecortin (an immature neuron marker)-positive new neurons. Furthermore, the dendritic complexity of the immature neurons was suppressed by DXM treatment. These findings suggest that DXM induces depression- and anxiety-like behavior and suppresses neurogenesis in rats. The current experimental paradigm may serve as an animal model for study on affective effect of cough mixture abuse, rehabilitation treatment options for abusers and the related neurological mechanisms.
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Depressão/induzido quimicamente , Depressão/patologia , Dextrometorfano/toxicidade , Antagonistas de Aminoácidos Excitatórios/toxicidade , Hipocampo/patologia , Neurogênese/efeitos dos fármacos , Animais , Peso Corporal/efeitos dos fármacos , Bromodesoxiuridina/metabolismo , Proliferação de Células/efeitos dos fármacos , Dendritos/metabolismo , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Proteínas do Domínio Duplacortina , Proteína Duplacortina , Comportamento Exploratório/efeitos dos fármacos , Relações Interpessoais , Masculino , Proteínas Associadas aos Microtúbulos/metabolismo , Neurônios/citologia , Neurônios/efeitos dos fármacos , Neuropeptídeos/metabolismo , Ratos , Ratos Sprague-Dawley , Natação/psicologia , Fatores de TempoRESUMO
Amauroderma rugosum (AR), also known as "Blood Lingzhi" in Chinese, is a basidiomycete belonging to the Ganodermataceae family. Four polysaccharide fractions were systematically isolated and purified from AR. Subsequently, their compositions were examined and analyzed via high-performance gel permeation chromatography (HPGPC), analysis of the monosaccharide composition, Fourier-transform infrared spectroscopy (FT-IR), and 1H nuclear magnetic resonance (NMR). The zebrafish model was then used to screen for proangiogenic activities of polysaccharides by inducing vascular insufficiency with VEGF receptor tyrosine kinase inhibitor II (VRI). The third fraction of AR polysaccharides (PAR-3) demonstrated the most pronounced proangiogenic effects, effectively ameliorating VRI-induced intersegmental vessel deficiency in zebrafish. Concurrently, the mRNA expression levels of vascular endothelial growth factor (VEGF)-A and VEGF receptors were upregulated by PAR-3. Moreover, the proliferation, migration, invasion, and tube formation of human umbilical vein endothelial cells (HUVECs) were also stimulated by PAR-3, consistently demonstrating that PAR-3 possesses favorable proangiogenic properties. The activation of the Akt, ERK1/2, p38 MAPK, and FAK was most likely the underlying mechanism. In conclusion, this study establishes that PAR-3 isolated from Amauroderma rugosum exhibits potential as a bioresource for promoting angiogenesis.
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Células Endoteliais da Veia Umbilical Humana , Peixe-Zebra , Animais , Humanos , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Movimento Celular/efeitos dos fármacos , Polissacarídeos/farmacologia , Polissacarídeos/química , Fator A de Crescimento do Endotélio Vascular/metabolismo , Fator A de Crescimento do Endotélio Vascular/genética , Neovascularização Fisiológica/efeitos dos fármacos , Indutores da Angiogênese/farmacologia , Indutores da Angiogênese/química , Receptores de Fatores de Crescimento do Endotélio Vascular/metabolismo , Receptores de Fatores de Crescimento do Endotélio Vascular/genética , Basidiomycota/química , Polissacarídeos Fúngicos/farmacologia , Polissacarídeos Fúngicos/químicaRESUMO
BACKGROUND: Amauroderma rugosum (AR) is a medicinal mushroom commonly used to treat inflammation, gastric disorders, epilepsy, and cancers due to its remarkable anti-inflammatory and anti-oxidative properties. This study was designed to evaluate the pharmacological effects of AR and its underlying mechanism of action against ulcerative colitis (UC) in vitro and in vivo. METHODS: A UC mouse model was established by administration of dextran sulfate sodium (DSS). AR extract was administered intragastrically to mice for 7 days. At the end of the experiment, histopathology, macrophage phenotype, oxidative stress, and inflammatory status were examined in vivo. Furthermore, RAW 264.7, THP-1, and Caco-2 cells were used to elucidate the mechanism of action of AR in vitro. RESULTS: AR extract (0.5-2â¯mg/mL) significantly suppressed lipopolysaccharide (LPS) and interferon-gamma (IFN-γ)-induced M1 macrophage (pro-inflammatory) polarization in both RAW 264.7 and THP-1 cells. LPS-induced pro-inflammatory mediators (nitric oxide, TNF-α, IL-1ß, MCP-1, and IL-6) were reduced by AR extract in a concentration-dependent manner. Similarly, AR extract downregulated MAPK signaling activity in LPS-stimulated RAW 264.7 cells. AR extract elicited a concentration-dependent increase in the mRNA expression of M2 (anti-inflammatory) phenotype markers (CD206, Arg-1, Fizz-1, and Ym-1) in RAW 264.7 cells. Moreover, AR extract suppressed DSS-induced ROS generation and mitochondrial dysfunction in Caco-2 cells. The in vivo experiment revealed that AR extract (200â¯mg/kg) increased colon length compared to the DSS-treated group. In addition, disease activity index, spleen ratio, body weight, oxidative stress, and colonic inflammation were markedly improved by AR treatment in DSS-induced UC mice. Finally, AR suppressed M1 and promoted M2 macrophage polarization in UC mice. CONCLUSION: The AR extract protected against DSS-induced UC by regulating macrophage polarization and suppressing oxidative stress. These valuable findings suggest that adequate intake of AR can prevent and/or treat UC.
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Colite Ulcerativa , Sulfato de Dextrana , Macrófagos , Estresse Oxidativo , Animais , Colite Ulcerativa/induzido quimicamente , Colite Ulcerativa/tratamento farmacológico , Colite Ulcerativa/patologia , Colite Ulcerativa/metabolismo , Colite Ulcerativa/prevenção & controle , Estresse Oxidativo/efeitos dos fármacos , Camundongos , Humanos , Células CACO-2 , Células RAW 264.7 , Macrófagos/efeitos dos fármacos , Macrófagos/metabolismo , Masculino , Células THP-1 , Anti-Inflamatórios/farmacologia , Modelos Animais de Doenças , Camundongos Endogâmicos C57BL , Citocinas/metabolismo , Mediadores da Inflamação/metabolismoRESUMO
Olfactory dysfunction and neuropsychiatric symptoms are commonly reported by patients of coronavirus disease 2019 (COVID-19), a respiratory infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Evidence from recent research suggests linkages between altered or loss of smell and neuropsychiatric symptoms after infection with the coronavirus. Systemic inflammation and ischemic injury are believed to be the major cause of COVID-19-related CNS manifestation. Yet, some evidence suggest a neurotropic property of SARS-CoV-2. This mini-review article summarizes the neural correlates of olfaction and discusses the potential of trans-neuronal transmission of SARS-CoV-2 or its particles within the olfactory connections in the brain. The impact of the dysfunction in the olfactory network on the neuropsychiatric symptoms associated with COVID-19 will also be discussed.
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Background: Autophagy is a conserved physiological intracellular mechanism responsible for the degradation and recycling of cytoplasmic constituents (e.g., damaged organelles, and protein aggregates) to maintain cell homeostasis. Aberrant autophagy has been observed in neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Amyotrophic Lateral Sclerosis (ALS), and Huntington's Disease (HD), and recently aberrant autophagy has been associated with mood disorders, such as depression. Several in vitro methods have been developed to study the complex and tightly regulated mechanisms of autophagy. In vitro methods applied to autophagy research are used to identify molecular key players involved in dysfunctional autophagy and to screen autophagy regulators with therapeutic applications in neurological diseases and mood disorders. Therefore, the aims of this narrative review are (1) to compile information on the cell-based methods used in autophagy research, (2) to discuss their application, and (3) to create a catalog of traditional and novel in vitro methods applied in neurodegenerative diseases and depression. Methods: Pubmed and Google Scholar were used to retrieve relevant in vitro studies on autophagy mechanisms in neurological diseases and depression using a combination of search terms per mechanism and disease (e.g., "macroautophagy" and "Alzheimer's disease"). A total of 37 studies were included (14 in PD, 8 in AD, 5 in ALS, 5 in %, and 5 in depression). Results: A repertoire of traditional and novel approaches and techniques was compiled and discussed. The methods used in autophagy research focused on the mechanisms of macroautophagy, microautophagy, and chaperone-mediated autophagy. The in vitro tools presented in this review can be applied to explore pathophysiological mechanisms at a molecular level and to screen for potential therapeutic agents and their mechanism of action, which can be of great importance to understanding disease biology and potential therapeutic options in the context of neurodegenerative disorders and depression. Conclusion: This is the first review to compile, discuss, and provide a catalog of traditional and novel in vitro models applied to neurodegenerative disorders and depression.
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SH3 and multiple ankyrin repeat domains protein (SHANK) 1, SHANK2, and SHANK3 encode a family of postsynaptic scaffolding proteins present at glutamatergic synapses and play a crucial role in synaptogenesis. In the past years, studies have provided a preliminary appreciation and understanding of the influence of the SHANK family in controlling stem cell fate. Here, we review the modulation of SHANK gene expression and their related signaling pathways, allowing for an in-depth understanding of the role of SHANK in stem cells. Besides, their role in governing stem cell self-renewal, proliferation, differentiation, apoptosis, and metabolism are explored in neural stem cells (NSCs), stem cells from apical papilla (SCAPs), and induced pluripotent stem cells (iPSCs). Moreover, iPSCs and embryonic stem cells (ESCs) have been utilized as model systems for analyzing their functions in terms of neuronal development. SHANK-mediated stem cell fate determination is an intricate and multifactorial process. This study aims to achieve a better understanding of the role of SHANK in these processes and their clinical applications, thereby advancing the field of stem cell therapy. This review unravels the regulatory role of the SHANK family in the fate of stem cells.
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Neurogênese , Sinapses , Células-TroncoRESUMO
It is widely acknowledged that the climacteric syndrome negatively affects women's quality of life and leads to cerebral ischemic injury, osteoporosis and cardiovascular disease. One of the main active ingredients in Radix Scutellariae, Baicalin, has been established to possess a wide range of pharmacological effects and is beneficial in enhancing osteogenic differentiation and cardiovascular disease. Baicalin's profound metabolic impact on various stem cell populations and their fate specification could improve the efficiency of stem cell therapy for climacteric syndrome. However, Baicalin-mediated processes are complex and many of the underlying mechanisms are not fully fathomed yet. This review aims to shed light on the regulatory role of Baicalin on the diverse behaviors of distinct stem cell populations and provide a good cell source for stem cell therapy to broaden the therapeutic landscape for climacteric syndrome patients.
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INTRODUCTION: Corticosterone inhibits male rodent sexual behavior while the mechanism remains obscured. Recent studies have disclosed that neurogenesis in the subventricular zone (SVZ) can be increased by pheromone exposure from the opposite sex, and neurogenesis is essential for normal mating behavior of female mice. Together with the neurogenesis-inhibiting effect of corticosterone, we hypothesize that cell proliferation in the olfactory system is essential for male rodent sexual functioning. AIM: The current study explored the relationship between cell proliferation in the olfactory system and male sexual behavior. MAIN OUTCOME MEASURES: Sexual behavior performance, proliferative cell counts, and c-fos-expressing cell counts. METHODS: Adult male rats were treated with corticosterone and/or paroxetine, an antidepressant, for 2 weeks. These two drugs were shown to suppress and enhance hippocampus and SVZ cell proliferation, respectively. Mating behavior was assessed after the treatment, and proliferation of new cells and c-fos-expressing cells, activated neurons in the mating-related regions in the brain, were analyzed. To further confirm the necessity of cell proliferation in mating, inhibition of cell proliferation was performed by intracerebroventricular infusion of cytostatic cytosine arabinose (Ara-c). RESULTS: Corticosterone treatment, which inhibited cell proliferation in both the SVZ and olfactory epithelium, led to inhibited male sexual performance. In contrast, paroxetine increased cell proliferation and improved the performance in corticosterone-treated animals. When cell proliferation in the brain was inhibited by Ara-c, a suppressed sexual performance was found. However, cell proliferation in olfactory epithelium was not inhibited by Ara-c and thus the sexual inhibition is unlikely to be linked to this region. Furthermore, a decrease in c-fos expression in the mating-related regions upon female pheromone stimulation was found. CONCLUSIONS: These results suggest that cell proliferation in the SVZ and hippocampus may be involved in the reproduction of the male rodents, and pharmacological treatments may affect sexual functioning through alteration of neurogenesis.
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Anti-Inflamatórios/farmacologia , Corticosterona/farmacologia , Neurogênese/efeitos dos fármacos , Paroxetina/farmacologia , Inibidores Seletivos de Recaptação de Serotonina/farmacologia , Comportamento Sexual Animal/efeitos dos fármacos , Animais , Proliferação de Células/efeitos dos fármacos , Corticosterona/antagonistas & inibidores , Citarabina/farmacologia , Masculino , Mucosa Olfatória/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Atrativos Sexuais/fisiologia , Comportamento Sexual Animal/fisiologiaRESUMO
BACKGROUND AND PURPOSE: Several studies have evaluated the effects of high-intensity aerobic training (HIAT) on pain severity and quality of life (QoL) among women with primary dysmenorrhea. However, to date, no studies have evaluated the effectiveness of HIAT on academic performance or absenteeism or examined the cost-effectiveness of HIAT relative to other treatments in women with primary dysmenorrhea. Furthermore, the mechanisms underlying aerobic exercise-induced analgesia in primary dysmenorrhea remain unclear. The objectives of this study are to: (1) evaluate the effects of HIAT on absenteeism and academic performance among university students, (2) identify the underlying mechanisms associated with aerobic exercise-induced analgesia in primary dysmenorrhea, and (3) determine the cost-effectiveness of HIAT compared with a wait-list control (WLC) group receiving usual care. METHODS: A sequential, embedded, mixed-methods study design, including a crossover, randomised controlled trial (RCT) and semi-structured focus groups, will be conducted alongside an economic evaluation. A total of 130 women aged 18-24 years will be randomised into either HIAT (n = 65) or wait-list control (n = 65) groups. Primary outcomes will include average pain intensity, absenteeism from university, and academic performance. Primary mediators will include salivary progesterone and prostaglandin F2α levels. Outcome and meditator variables will be assessed at baseline and post-treatment, at 12 and 28 weeks. An economic analysis will be conducted from the societal and healthcare perspective of Hong Kong. Semi-structured focus groups will be conducted at 32 weeks. Of the 130 participants included in the RCT, 70 will be included in the focus groups. STATISTICAL ANALYSIS: All statistical analyses will be performed on an intention-to-treat basis, using SPSS (version 24). Preliminary analysis using an independent samples t-test and a two-sided, unpaired Student's t-test will be performed to exclude carryover effects and identify within-participant differences in outcome variables between the study periods, respectively. Treatment effects will be evaluated using analysis of variance via a mixed-effects model with fixed effects for intervention, period, and sequence. In all models, random effects will include the participants nested within the sequence as a sampling cluster. The mediation effects will be assessed using the Sobel test. The EQ-5D responses will be converted into utility scores to estimate the gain or loss of quality-adjusted life-years. Seemingly unrelated regression analyses will be used to estimate the total cost differences and effect differences. Qualitative data will be analysed using the process of thematic analysis.
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Análise Custo-Benefício/estatística & dados numéricos , Dismenorreia/prevenção & controle , Exercício Físico , Dor/prevenção & controle , Absenteísmo , Desempenho Acadêmico/estatística & dados numéricos , Adolescente , Estudos Cross-Over , Dinoprosta/metabolismo , Dismenorreia/metabolismo , Dismenorreia/fisiopatologia , Estudos de Viabilidade , Feminino , Grupos Focais , Humanos , Dor/metabolismo , Dor/fisiopatologia , Progesterona/metabolismo , Qualidade de Vida/psicologia , Anos de Vida Ajustados por Qualidade de Vida , Ensaios Clínicos Controlados Aleatórios como Assunto , Estudantes , Universidades , Adulto JovemRESUMO
Previous studies have demonstrated that a non-invasive light-flickering regime and auditory tone stimulation could affect Aß and tau metabolism in the brain. As a non-invasive technique, repetitive transcranial magnetic stimulation (rTMS) has been applied for the treatment of neurodegenerative disorders. This study explored the effects of rTMS on Aß and tau levels in rhesus monkey cerebrospinal fluid (CSF). This is a single-blind, self-controlled study. Three different frequencies (low frequency, 1 Hz; high frequencies, 20 Hz and 40 Hz) of rTMS were used to stimulate the bilateral-dorsolateral prefrontal cortex (DLPFC) of the rhesus monkey. A catheterization method was used to collect CSF. All samples were subjected to liquid chip detection to analyze CSF biomarkers (Aß42, Aß42/Aß40, tTau, pTau). CSF biomarker levels changed with time after stimulation by rTMS. After stimulation, the Aß42 level in CSF showed an upward trend at all frequencies (1 Hz, 20 Hz, and 40 Hz), with more significant differences for the high-frequencies (p < 0.05) than for the low frequency. After high-frequency rTMS, the total Tau (tTau) level of CSF immediately increased at the post-rTMS timepoint (p < 0.05) and gradually decreased by 24 h. Moreover, the results showed that the level of phosphorylated Tau (pTau) increased immediately after 40 Hz rTMS (p < 0.05). The ratio of Aß42/Aß40 showed an upward trend at 1 Hz and 20 Hz (p < 0.05). There was no significant difference in the tau levels with low-frequency (1 Hz) stimulation. Thus, high-frequencies (20 Hz and 40 Hz) of rTMS may have positive effects on Aß and tau levels in rhesus monkey CSF, while low-frequency (1 Hz) rTMS can only affect Aß levels.
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Córtex Pré-Frontal , Estimulação Magnética Transcraniana , Animais , Macaca mulatta , Projetos Piloto , Método Simples-CegoRESUMO
INTRODUCTION: Coronavirus disease 2019 (COVID-19) has led to radical changes in social distancing awareness and affected social relationships. Owing to large-scale lockdown, home quarantine and social distancing requirements, it was anticipated that sexual activities would be severely impacted. However, retrospective self-report studies showed that pornography use and autoerotism increased during the pandemic. AIM: This study used big-data databases available on the Internet to investigate factors that modulated pornography use during the pandemic. METHODS: Daily relative search volume (RSV) data from Google Trends for the period from 24 February 2020 to 13 July 2020 were extracted. Pornhub traffic data were extracted from the Pornhub Insights website, for the period from 24 February 2020 to 13 July 2020. The parameter was defined as 'percent change in traffic compared to an average day in 2019'. The number of daily new cases of COVID-19 was extracted from the database on Our World in Data. OUTCOME MEASURES: The normality of the data was examined using the Shapiro-Wilk test. All variables included in this study were non-normally distributed. Therefore, non-parametric tests or parametric tests with bootstrapping were adopted where appropriate. RESULTS: According to Google Trends, the RSV for 'pornography' increased after late March 2020, which is close to the date when the World Health Organization declared COVID-19 a global pandemic. The number of daily new cases of COVID-19 was positively correlated with the traffic of Pornhub, a popular pornography website, and the RSV for 'pornography'. Moderation analysis demonstrated a significant main effect of daily new cases of COVID-19 and the RSV for 'social distancing' in predicting Pornhub traffic/RSV for 'pornography'. Furthermore, the RSV for 'social distancing' significantly moderated the relationship between daily new cases and Pornhub traffic/RSV for 'pornography'. A stronger COVID-pornography use association was observed with increased social distancing awareness. CONCLUSION: Increased pornography consumption during the pandemic was observed, and it was associated with the severity of the pandemic. Social distancing awareness could be a key factor influencing interest in and use of pornography. Further studies on the changes in sexual desire and birth-rate control are worthwhile because long-term public health may be affected by the changes in sexual behaviour during the pandemic.
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COVID-19/epidemiologia , Literatura Erótica , Uso da Internet/estatística & dados numéricos , Big Data , COVID-19/psicologia , Humanos , Distanciamento Físico , Análise de RegressãoRESUMO
Extremely low frequency electromagnetic fields (ELF-EMF) can improve the learning and memory impairment of rats with Alzheimer's disease, however, its effect on cerebral ischemia remains poorly understood. In this study, we established rat models of middle cerebral artery occlusion/reperfusion. One day after modeling, a group of rats were treated with ELF-EMF (50 Hz, 1 mT) for 2 hours daily on 28 successive days. Our results showed that rats treated with ELF-EMF required shorter swimming distances and latencies in the Morris water maze test than those of untreated rats. The number of times the platform was crossed and the time spent in the target quadrant were greater than those of untreated rats. The number of BrdU+/NeuN+ cells, representing newly born neurons, in the hippocampal subgranular zone increased more in the treated than in untreated rats. Up-regulation in the expressions of Notch1, Hes1, and Hes5 proteins, which are the key factors of the Notch signaling pathway, was greatest in the treated rats. These findings suggest that ELF-EMF can enhance hippocampal neurogenesis of rats with cerebral ischemia, possibly by affecting the Notch signaling pathway. The study was approved by the Institutional Ethics Committee of Sichuan University, China (approval No. 2019255A) on March 5, 2019.
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Transcranial magnetic stimulation, a type of noninvasive brain stimulation, has become an ancillary therapy for motor function rehabilitation. Most previous studies have focused on the effects of repetitive transcranial magnetic stimulation (rTMS) on motor function in stroke patients. There have been relatively few studies on the effects of different modalities of rTMS on lower extremity motor function and corticospinal excitability in patients with stroke. The MEDLINE, Embase, Cochrane Library, ISI Science Citation Index, Physiotherapy Evidence Database, China National Knowledge Infrastructure Library, and ClinicalTrials.gov databases were searched. Parallel or crossover randomized controlled trials that addressed the effectiveness of rTMS in patients with stroke, published from inception to November 28, 2019, were included. Standard pairwise meta-analysis was conducted using R version 3.6.1 with the "meta" package. Bayesian network analysis using the Markov chain Monte Carlo algorithm was conducted to investigate the effectiveness of different rTMS protocol interventions. Network meta-analysis results of 18 randomized controlled trials regarding lower extremity motor function recovery revealed that low-frequency rTMS had better efficacy in promoting lower extremity motor function recovery than sham stimulation. Network meta-analysis results of five randomized controlled trials demonstrated that high-frequency rTMS led to higher amplitudes of motor evoked potentials than low-frequency rTMS or sham stimulation. These findings suggest that rTMS can improve motor function in patients with stroke, and that low-frequency rTMS mainly affects motor function, whereas high-frequency rTMS increases the amplitudes of motor evoked potentials. More high-quality randomized controlled trials are needed to validate this conclusion. The work was registered in PROSPERO (registration No. CRD42020147055) on April 28, 2020.
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Altered sensory processing and perception has been one of the characteristics of autism spectrum disorder (ASD). In this chapter, we review the neural underpinnings of sensory abnormalities of ASD by examining the literature on clinical, behavioral and neurobiological evidence that underlies the main patterns of sensory integration function and dysfunction. Furthermore, neural differences in anatomy, function and connectivity of different regions underlying sensory processing are also discussed. We conclude that sensory integration intervention is built on the premise of neuroplasticity to improve function and behavior for individuals with ASD.
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Transtorno do Espectro Autista/fisiopatologia , Percepção , Humanos , Plasticidade Neuronal/fisiologia , SensaçãoRESUMO
The popular accepted explanation for the pathogenesis of primary dysmenorrhea is elevated levels of uterine prostaglandins. Aetiological studies report that production of prostaglandins is controlled by the sex hormone progesterone, with prostaglandins and progesterone displaying an inverse relationship (i.e. increased progesterone levels reduce prostaglandin levels). Pro-inflammatory cytokines (interleukin-6 [IL-6] and tumor necrosis factor-alpha [TNF-α]) are also implicated in the pathogenesis of primary dysmenorrhea. High-intensity aerobic exercise is effective for decreasing pain quality and intensity in women with primary dysmenorrhea. However, why and how aerobic exercise is effective for treatment of primary dysmenorrhea remain unclear. Our preliminary non-randomized controlled pilot study to examine the effects of high-intensity aerobic exercise on progesterone, prostaglandin metabolite (13,14-dihydro-15-keto-prostaglandin F2 alpha (KDPGF2α), TNF-α, and pain intensity found increases in progesterone and decreases in KDPGF2α, TNF-α, and pain intensity following high-intensity aerobic exercise relative to no exercise. Given these promising preliminary findings, as well as what is known about the pathogenesis of primary dysmenorrhea, we propose the following scientific hypothesis: high-intensity aerobic exercise utilizes hormone (progesterone) and inflammatory cytokine-mediated mechanisms to reduce the pain associated with primary dysmenorrhea.
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Citocinas/metabolismo , Dismenorreia/metabolismo , Exercício Físico , Manejo da Dor/métodos , Progesterona/metabolismo , Prostaglandinas/metabolismo , Dinoprosta/análogos & derivados , Dinoprosta/metabolismo , Dismenorreia/sangue , Feminino , Hormônios/metabolismo , Humanos , Inflamação , Projetos Piloto , Útero/metabolismoRESUMO
Cerebral ischemic injury is the main manifestation of stroke, and its incidence in stroke patients is 70-80%. Although ischemic stroke can be treated with tissue-type plasminogen activator, its time window of effectiveness is narrow. Therefore, the incidence of paralysis, hypoesthesia, aphasia, dysphagia, and cognitive impairment caused by cerebral ischemia is high. Nerve tissue regeneration can promote the recovery of the aforementioned dysfunction. Neural stem cells can participate in the reconstruction of the damaged nervous system and promote the recovery of nervous function during self-repair of damaged brain tissue. Neural stem cell transplantation for ischemic stroke has been a hot topic for more than 10 years. This review discusses the treatment of ischemic stroke with neural stem cells, as well as the mechanisms of their involvement in stroke treatment.
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Background: The exact mechanisms involved in the pathogenesis of neurodegenerative conditions are not fully known. The design of drugs that act on multiple targets represents a promising approach that should be explored for more effective clinical options for neurodegenerative disorders. B7C is s synthetic drug that has been studied for over 20 years and represents a promising multi-target drug for the treatment of neurodegenerative disorders, such as AD. Aims: The present systematic review, thus, aims at examining existing studies on the effect of B7C on different molecular targets and at discussing the relevance of B7C in neurological disorders. Methods: A list of predefined search terms was used to retrieve relevant articles from the databases of Embase, Pubmed, Scopus, and Web of Science. The selection of articles was done by two independent authors, who were considering articles concerned primarily with the evaluation of the effect of B7C on neurological disorders. Only full-text articles written in English were included; whereas, systematic reviews, meta-analyses, book chapters, conference subtracts, and computational studies were excluded. Results: A total of 2,266 articles were retrieved out of which 41 articles were included in the present systematic review. The effect of B7C on molecular targets, including AChE, BChE, BACE-1, NMDA receptor, GABA receptor, NOS, and Kv4.2 potassium channels was evaluated. Moreover, the studies that were included assessed the effect of B7C on biological processes, such as apoptosis, neuritogenesis, and amyloid beta aggregation. The animal studies examined in the review focused on the effect of B7C on cognition and memory. Conclusions: The beneficial effects observed on different molecular targets and biological processes relevant to neurological conditions confirm that B7C is a promising multi-target drug with the potential to treat neurological disorders.
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Depression is a major health issue that causes severe societal economic and health burden. Aromatherapy, a practice that uses essential oils for preventive and therapeutic purposes, represents a promising therapeutic alternative for the alleviation of depressive symptoms. Lavender essential oil (LEO) has been the focus of clinical studies due to its positive effect on mood. An animal model of chronic administration of high dose corticosterone to induce depression- and anxiety-like behavior and reduced neurogenesis was used to explore the biological changes brought by aromatherapy. Twenty-four adult male Sprague Dawley rats were randomly assigned into four groups: Control, corticosterone (Cort) group with high dose of corticosterone, LEO group with daily exposure to LEO by inhalation, and LEO + Cort. At the end of the 14-day treatment period, behavioral tests were carried out. Serum samples were collected 2-3 days after the 14-day period treatment and before perfusion to carry out biochemical analyses to measure BDNF, corticosterone and oxytocin. After perfusion, brains were collected for immunohistochemical analysis to detect BrdU and DCX positive cells in the hippocampus and subventricular zone. Results showed that treatment with LEO ameliorated the depression-like behavior induced by the chronic administration of corticosterone as observed in the LEO + Cort group. Cort treatment reduced the number of BrdU positive cells in the hippocampus and the subventricular zone. Treatment with LEO prevented the corticosterone-induced reduction in the number of BrdU positive cells (LEO + Cort group) demonstrating the neurogenic effect of LEO under high corticosterone conditions. Chronic administration of high dose of corticosterone significantly reduced the dendritic complexity of immature neurons. On the contrary, treatment with LEO increased dendritic complexity of immature neurons under high corticosterone conditions (LEO + Cort group). The improved neurogenesis and dendritic complexity observed in the LEO + Cort group demonstrated a clear restorative effect of LEO under high corticosterone conditions. However, 2-3 days after the treatment, the levels of BDNF were upregulated in the LEO and LEO + Cort groups. Furthermore, the concentration of oxytocin in serum, 2-3 days after the treatment, showed to be upregulated in the LEO group alone. The present study has provided evidence of the biological effect of LEO on neuroplasticity and neurogenesis. Also, this study contributes to the understanding of the mechanism of action of LEO in an animal model where depression- and anxiety-like behavior and reduced neurogenesis were induced by high corticosterone administration.