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How long for cbd oil to work for anxiety without

Quevedo João

Grek63
27.10.2018

Content:

  • Quevedo João
  • João Quevedo
  • Manage My Suggestions
  • Biography. João Luciano de Quevedo, MD, PhD, is professor and vice chair of Faculty Development and Outreach in the Department of Psychiatry and. Dr. Joao de Quevedo. Dr. Quevedo's lab (Translational Psychiatry Program) is engaged in preclinical research in the field of psychiatry. These studies involve. Joao Quevedo of University of Texas Health Science Center at Houston, Texas ( UT Houston). Read publications, and contact Joao Quevedo on.

    Quevedo João

    The modified Yale Food Addiction Scale 2. However, there is no validated instrument to assess food addiction. The data for this study was obtained through an anonymous web-based research platform: Overall, 7, participants were included A single factor solution yielded the best goodness-of-fit parameters for both the continuous and categorical version of the mYFAS 2.

    In addition, mYFAS 2. Maternal deprivation MD induces behavioral changes and impacts brain circuits that could be associated with the pathophysiology of depression. This study investigated the markers of microglia and astrocyte activation as well as indoleamine 2,3-dioxygenase IDO expression in developmental programming after early life MD on postnatal days PNDs 20, 30, 40, and On PND 10, it was found that there was a decrease in the level of glial fibrillary acidic protein GFAP immunopositive cells, a decrease in the level of IDO expression, and an increase in the level of Iba-1 microglial marker in the hippocampus of rats that were subjected to MD.

    On PND 30, the levels of Iba-1 remained elevated. These results suggest that early life stress induces negative developmental programming in rats, as demonstrated by depressive-like behavior in adult life.

    Moreover, MD increases microglial activation in both early and late developmental phases. These findings suggest that MD could differentially affect the expression of the IDO enzyme, astrocytes, and microglial activation depending on the neurodevelopmental period. The onset of an inflammatory state from resident brain cells could be associated with the activation of the kynurenine pathway and the development of depressive behavior in adulthood. Evaluation of plasma biomarkers of inflammation in patients with maple syrup urine disease.

    Maple syrup urine disease MSUD is an autosomal recessive inherited disorder that affects branched-chain amino acid BCAA catabolism and is associated with acute and chronic brain dysfunction. Recent studies have shown that inflammation may be involved in the neuropathology of MSUD.

    However, these studies have mainly focused on single or small subsets of proteins or molecules. Here we performed a case-control study, including 12 treated-MSUD patients, in order to investigate the plasmatic biomarkers of inflammation, to help to establish a possible relationship between these biomarkers and the disease.

    Overall, data reported here are consistent with the working hypothesis that inflammation may be involved in the pathophysiological mechanism underlying the brain damage observed in MSUD patients. Objective Evidence suggests that skin picking disorder SPD could be a prevalent condition associated with comorbidity and psychosocial dysfunction. However, just a few studies have assessed the prevalence and correlates of SPD in samples from low- and middle-income countries.

    In addition, the impact of SPD on quality of life QoL dimension after multivariable adjustment to potential confounders remains unclear. Methods Data were obtained from a Brazilian anonymous Web-based research platform. Associations were adjusted to potential confounders through multivariable models. Results For our survey, participants took part The prevalence of SPD was 3. In addition, SPD was associated with a positive screen for a major depressive episode, nicotine dependence, and alcohol dependence, as well as suicidal ideation.

    Physical and psychological QoL was significantly more impaired in participants with SPD compared to those without SPD, even after adjustment for comorbidity. Conclusions In this large sample, SPD was a prevalent condition associated with co-occurring depression, nicotine, and alcohol dependence. Public health efforts toward the early recognition and treatment of SPD are warranted.

    Evidence for additionally increased apoptosis in the peripheral blood mononuclear cells of major depressive patients with a high risk for suicide. Several studies have suggested a pathophysiological role of blood cell apoptosis in major depressive disorder MDD.

    Our findings may support the role of both internal and external apoptotic pathways in the interplay between the immune system and depressive symptoms, especially in patients with a high risk for suicide. Increased oxidative stress in the mitochondria isolated from lymphocytes of bipolar disorder patients during depressive episodes.

    The present study aims to investigate the oxidative stress parameters in isolated mitochondria, as well as looking at mitochondrial complex activity in patients with Bipolar Disorder BD during depressive or euthymic episodes.

    We evaluated the following oxidative stress parameters: Our results indicated that the depressive phase could increase the levels of mitochondrial superoxide, carbonyl and TBARS, and superoxide dismutase, and could decrease the levels of mitochondrial complex II activity in the lymphocytes of bipolar patients.

    Additionally, there was a negative correlation between complex II activity and oxidative stress parameters. In conclusion, our results suggest that mitochondrial oxidative stress and mitochondrial complex II dysfunction play important roles in the depressive phase of BD. Sepsis is systemic inflammatory response syndrome with a life-threatening organ dysfunction that is caused by an unbalanced host immune response in an attempt to eliminate invasive microorganisms.

    A total of papers were included in the primary screening. After that, articles were selected for the study. In addition, the rodents presented long-term cognitive impairment in different behavioral tasks that were prevented by blocking the mechanism of action of these inflammatory mediators.

    Clinical studies have showed that sepsis survivors presented increased bodily symptoms such as fatigue, pain, visual disturbances, gastrointestinal problems, and neuropsychiatric problems compared to before sepsis. Sepsis leaves the survivors with an aftermath of physiological, neuropsychiatric, and functional impairment. The role of memantine in the treatment of major depressive disorder: Clinical efficacy and mechanisms of action.

    A developing body of evidence indicates that disturbed glutamate neurotransmission especially through N-methyl-d-aspartate NMDA is central to the pathophysiology of major depressive disorder MDD and NMDA receptor antagonists have shown therapeutic potential in the MDD treatment.

    Memantine is an uncompetitive NMDA receptor antagonist, approved for treatment of Alzheimer's disease AD that in contrast to other NMDA receptor antagonists at therapeutic doses does not induce highly undesirable side effects.

    Neuroprotective properties and well tolerability of memantine have been attributed to its unique pharmacological features such as moderate affinity, rapid blocking kinetics and strongly voltage-dependency. In this review we summarized clinical trial evidence of antidepressant effectiveness of memantine and its mechanisms of action. Available data indicate contradictory findings relating to clinical efficacy suggesting further research is necessary in determining as to whether memantine will eventually be an advantageous therapy for MDD.

    Preclinical data proposed various neurobiological mechanisms underlying antidepressant-like properties of memantine that are responsible for synaptic plasticity and cell survival.

    Intravenous infusion of xenon-containing liposomes generates rapid antidepressant-like effects. Similar to ketamine, xenon gas acts as a glutamatergic N-methyl-d-aspartate receptor antagonist, but devoid of propensity to cause untoward effects.

    The uncaging of xenon gas from circulating Xe-liposome was facilitated by continuous ultrasound application externally on the neck over the internal common carotid artery.

    One-hour after Xe-liposome infusion, animals were assessed for depression-like behaviors using a forced swimming test FST , and spontaneous locomotor activity. This behavioral discrepancy was not associated with locomotion aberrations, as gross activity of rats remained similar for both doses. Omega-3 and folic acid act against depressive-like behavior and oxidative damage in the brain of rats subjected to early or late life stress. To investigate the antidepressant and antioxidant effects of omega-3, folic acid and n-acetylcysteine NAC in rats which were subjected to early or late life stress.

    Early stress was induced through maternal deprivation MD , while late life stress was induced using the chronic mild stress CMS protocol.

    Young rats which were subjected to MD and the adult rats which were subjected to CMS were treated with omega-3 fatty acids 0. Then, the animals' immobility times were evaluated using the forced swimming test. Oxidative stress parameters were evaluated in the brain.

    NAC, folic acid and omega-3 increased superoxide dismutase and catalase activities in the rat brain subjected to early or late life stress. NAC, omega-3 and folic acid may present interesting lines of treatment based on their antioxidant properties, which cause an inhibition of behavioral and brain changes that occur from stressful life events.

    This chapter will discuss the potential use of microRNAs, particularly those located in peripherally-isolated exosomes, as biomarkers in neuropsychiatric disorders. These extracellular vesicles are released as a form of cell-to-cell communication and may mediate the soma-to-germline transmission of brain-relevant information, thereby potentially contributing to the inter- or transgenerational transmission of behavioral traits.

    Recent novel methods allow for the enrichment of peripheral exosomes specifically released by neurons and astrocytes and may provide valuable brain-relevant biosignatures of disease. Tyrosinemia type II is an inborn error of metabolism caused by a deficiency in the activity of the enzyme tyrosine aminotransferase, leading to tyrosine accumulation in the body. Although the mechanisms involved are still poorly understood, several studies have showed that higher levels of tyrosine are related to oxidative stress and therefore may affect the cholinergic system.

    Thus, the aim of this study was to investigate the effects of chronic administration of L-tyrosine on choline acetyltransferase activity ChAT and acetylcholinesterase AChE in the brain of rats. Our results showed that the chronic administration of L-tyrosine decreases the ChAT activity in the cerebral cortex, while the AChE activity was increased in the hippocampus, striatum, and cerebral cortex.

    Moreover, we found that the antioxidant treatment was able to prevent the decrease in the ChAT activity in the cerebral cortex. However, the increase in AChE activity induced by L-tyrosine was partially prevented the in the hippocampus and striatum, but not in the cerebral cortex. Our results also showed no differences in the aversive and spatial memory after chronic administration of L-tyrosine.

    In conclusion, the results of this study demonstrated an increase in AChE activity in the hippocampus, striatum, and cerebral cortex and an increase of ChAT in the cerebral cortex, without cognitive impairment. Furthermore, the alterations in the cholinergic system were partially prevented by the co-administration of NAC and DFX. Thus, the restored central cholinergic system by antioxidant treatment further supports the view that oxidative stress may be involved in the pathophysiology of tyrosinemia type II.

    Second generation antipsychotic-induced mitochondrial alterations: Implications for increased risk of metabolic syndrome in patients with schizophrenia. Metabolic syndrome MetS is seen more frequently in persons with schizophrenia than in the general population, and these metabolic abnormalities are further aggravated by second generation antipsychotic SGA drugs. Although the underlying mechanisms responsible for the increased prevalence of MetS among patients under SGA treatment are not well understood, alterations in mitochondria function have been implicated.

    We performed a comprehensive evaluation of the role of mitochondrial dysfunction in the pathophysiology of drug-induced MetS in schizophrenia. We found a downregulation in genes encoding subunits of the electron transport chain complexes ETC , enzyme activity, and mitochondrial dynamics in peripheral blood cells from patients at high-risk for MetS. Additionally, we evaluated several markers of energy metabolism in lymphoblastoid cell lines from patients with schizophrenia and controls following exposure to antipsychotics.

    We found that the high-risk drugs clozapine and olanzapine induced a general down-regulation of genes involved in the ETC, as well as decreased activities of the corresponding enzymes, ATP levels and a significant decrease in all the functional parameters of mitochondrial oxygen consumption in cells from patients and controls.

    We also observed that the medium-risk SGA quetiapine decreased oxygen consumption and respiratory control ratio in controls and patients. Additionally, clozapine and olanzapine induced a downregulation of Drp1 and Mfn2 both in terms of mRNA and protein levels. Together, these data suggest that an intrinsic defect in multiple components of oxidative metabolism may contribute to the increased prevalence of MetS in patients under treatment with SGAs known to cause risk for MetS.

    Treatment with cannabidiol reverses oxidative stress parameters, cognitive impairment and mortality in rats submitted to sepsis by cecal ligation and puncture. A New Target of Depression. Jan Understanding Depression. Major depressive disorder MDD is a severe psychiatric condition that affects a large number of individuals worldwide.

    The understanding of the pathophysiology of this disorder is still not well elucidated, and considering that acute availability of monoamines in the synapses does not provide an equally acute response, and a large number of patients do not respond satisfactorily, new research has emerged in the search for markers and biological mechanisms underlying MDD.

    Clinical and experimental studies have been suggesting that mammalian target of rapamycin mTOR signaling is compromised in pathophysiology of MDD. In addition, this pathway is required for the rapid antidepressant action of ketamine, an antagonist of N-methyl-d-aspartate NMDA receptor. Thus, this chapter will highlight clinical and experimental evidences of the role of mTOR signaling pathway in the pathophysiology and treatment of MDD. Staging models and neuroprogression in bipolar disorder.

    Jan Bipolar Disorder Vulnerability. Animal Models of Mood Disorders: Focus on Bipolar Disorder and Depression. According to the Diagnostic and Statistical Manual of Mental Disorders Fifth Edition DSM-5 , the two major mood disorders are major depression MD and bipolar disorder BD ; however, despite receiving adequate treatment, most patients continue to have recurrent mood episodes and residual symptoms.

    The advances in genetic, neurobiological, and pharmacological methodologies have helped in the development of animal models, and these models have been an important tool for investigating new intracellular systems that may be involved in the specific pathophysiology of psychiatric disorders and, consequently, new therapeutic approaches.

    Valid animal models in psychiatric disorders should demonstrate the following three major criteria: This chapter seeks to provide a comprehensive overview of traditional and recent animal models for mania and depression, and methods to evaluate depressive- and manic-like behavior in animals, recapitulating their different features, and the possible pathophysiology of mood disorders emulated by those models.

    Accelerated epigenetic aging and mitochondrial DNA copy number in bipolar disorder. Bipolar disorder BD has been previously associated with accelerated aging; yet, the mechanisms underlying this association are largely unknown.

    The epigenetic clock has been increasingly recognized as a valuable aging marker, although its association with other biological clocks in BD patients and high-risk subjects, such as telomere length and mitochondrial DNA mtDNA copy number, has never been investigated. We included 22 patients with BD I, 16 siblings of BD patients, and 20 healthy controls in this analysis. DNA methylation age DNAm age and accelerated aging were calculated using the Horvath age estimation algorithm in blood and in postmortem brain from BD patients and nonpsychiatric controls using publicly available data.

    Older BD patients presented significantly accelerated epigenetic aging compared to controls, whereas no difference was detected among the younger subjects. Patients showed higher levels of mtDNA copy number, while no difference was found between controls and siblings.

    Telomere length did not show significant differences between groups, nor did it correlate with epigenetic aging or mtDNA copy number. These results suggest that BD may involve an accelerated epigenetic aging, which might represent a novel target for treating BD and subjects at risk. In particular, our results suggest a complex interplay between biological clocks to determine the accelerated aging and its consequences in BD.

    Acute treatment with ketamine and chronic treatment with minocycline exert antidepressant-like effects and antioxidant properties in rats subjected different stressful events. Despite decades of research, the fundamental neurochemical and molecular mechanisms underlying the major depressive disorder MDD are still poorly understood, and current antidepressant treatments have limited clinical efficacy.

    In clinical conditions, the rapprochement between the disease and the corrective actions of drugs in laboratory animals is essential for developing effective therapies. Thus, the aim of this study was to evaluate the antidepressant effects of ketamine N-metil-d-asparte NMDA receptor antagonist , minocycline tetracycline antibiotic , and amitriptyline classical antidepressant , on behavior and oxidative stress parameters in animals submitted to the chronic mild stress CMS and maternal deprivation protocols.

    For this aim, male Wistar rats were submitted to maternal deprivation or CMS. To induce maternal deprivation, Wistar rats were deprived of maternal care during the first 10 days of life. After treatment, the animals were submitted to the forced swimming test and then analyzed oxidative stress parameters in the prefrontal cortex PFC , hippocampus, amygdala and nucleus accumbens NAc.

    Treatment with ketamine, minocycline and amitriptyline were able to exert antidepressant effects in the forced swimming test.

    However, these antidepressant effects were dependent on the stress model by which the animals were exposed. In certain brain regions some treatment strategies had a pro-oxidant effect. In addition, an increase in the antioxidant superoxide dismutase SOD and catalase CAT enzymes activities were also evident after treatments. In conclusion, the antidepressant effects of ketamine and minocycline, in the present study, may be associated, at least in part, with its antioxidant and neuroprotective effects in animals subjected to maternal deprivation or CMS.

    The use of quetiapine in the treatment of major depressive disorder: Evidence from clinical and experimental studies. Major depressive disorder MDD is a highly debilitating condition that is drawing considerable attention due to its high global prevalence and to the fact that treatments are still far from reaching the total number of patients affected.

    Among available treatment strategies, quetiapine is an important research target, due to antidepressant responses in patients resistant to classical treatments and in animals submitted to protocols that induce depressive-like behaviours. Quetiapine has a broad spectrum of action, within which are many mechanisms that seem to be related to the most effective antidepressant therapeutic responses.

    In this review, research results related to the pharmacokinetic profile, neurotransmitters, receptors and signalling molecular targets involved in the functional and structural plasticity of key brain regions in MDD are reported and discussed. Moreover, the physiological mechanisms, which are targets of quetiapine and are involved in both MDD and poor therapeutic response, are reported. The main adverse effects observed from therapeutic dosages and overdose are also described.

    Finally, the main mechanisms underlying the therapeutic response are highlighted. Patients recovering from sepsis have higher rates of CNS morbidities associated with long-lasting impairment of cognitive functions, including neurodegenerative diseases.

    However, the molecular etiology of these sepsis-induced impairments is unclear. Here, we investigated the role of the receptor for advanced glycation end products RAGE in neuroinflammation, neurodegeneration-associated changes, and cognitive dysfunction arising after sepsis recovery.

    Adult Wistar rats underwent cecal ligation and perforation CLP , and serum and brain hippocampus and prefrontal cortex samples were obtained at days 1, 15, and 30 after the CLP.

    These results indicate that brain RAGE is an essential factor in the pathogenesis of neurological disorders following acute systemic inflammation. The additive effect of aging on sepsis-induced cognitive impairment and neuroinflammation. Systemic inflammation is emerging as a significant driver of cognitive decline in the aged and vulnerable brain. In sepsis survivors animals low-grade brain inflammation occurs, suggesting that sepsis is able to induce in microglia a primed-like state.

    The purpose of this study is to analyze the role of sepsis-induced brain inflammation in the progression of the physiological process of brain aging.

    In conclusion, neuroinflammation is persistent after sepsis and this could burst the usual inflammation that occurs during brain aging. The aim of this study was to investigate the effects of lithium on brain-derived neurotrophic factor BDNF , nerve growth factor NGF , and glial cell line-derived neurotrophic factor GDNF expression in the hippocampus and on memory in experimental pneumococcal meningitis.

    The mood-stabilizer lithium is known as a neuroprotective agent with many effects on the brain. Eighteen hours after induction, all animals received ceftriaxone. The animals received saline or lithium Ten days after meningitis induction, animals were subjected to open-field habituation and the step-down inhibitory avoidance tasks. In the meningitis group, treatment with lithium and tamoxifen resulted in improvement in memory. Lithium was able to prevent memory impairment and reestablishes hippocampal neurotrophin expression in experimental pneumococcal meningitis.

    Prevalence, psychopathological correlates and associations with quality of life in a large sample. Objective To determine the prevalence of food addiction in a large Brazilian non-clinical sample.

    Sociodemographic and psychopathological correlates of food addiction as well as associations with quality QoL domains were also investigated.

    Participants provided sociodemographic data and completed the modified Yale Food Addiction Scale 2. Results The prevalence of food addiction was 4. Conclusions Food addiction may be common in low and middle-income countries, though possibly less prevalent than in the US.

    Food addiction was associated with co-occurring mood disorders and skin picking disorder as well as with early life psychological and sexual abuse.

    Finally, food addiction was independently associated with broad reductions in QoL. Public health efforts towards the early recognition and management of food addiction are warranted. A Review of the Current Literature. Bipolar disorder BD is a major health problem. It causes significant morbidity and imposes a burden on the society.

    Thus, there is a great need to further our understanding the pathophysiology of BD to identify new therapeutic avenues. We present recent advances from preclinical and clinical studies that further support the role of PKC. The recent development of animal models of BD, such as stimulant-treated and paradoxical sleep deprivation, and the ability to intervene pharmacologically provide further insights into the involvement of PKC in BD.

    In addition, the effect of PKC inhibitors, such as tamoxifen, in the resolution of manic symptoms in patients with BD further points in that direction. Furthermore, a wide variety of growth factors influence neurotransmission through several molecular pathways that involve downstream effects of PKC.

    The inhibition of the kynurenine pathway prevents behavioral disturbances and oxidative stress in the brain of adult rats subjected to an animal model of schizophrenia. Evidence has shown that the kynurenine pathway KP plays a role in the onset of oxidative stress and also in the pathophysiology of schizophrenia. The aim of this study was to use a pharmacological animal model of schizophrenia induced by ketamine to investigate if KP inhibitors could protect the brains of Wistar rats against oxidative stress and behavioral changes.

    In addition, the IDO inhibitor prevented lipid peroxidation, and decreased the levels of protein carbonyl in the prefrontal cortex PFC , hippocampus and striatum.

    It also increased the activity of superoxide dismutase SOD in the hippocampus, as well as increasing the levels of catalase activity in the PFC and hippocampus. The TDO inhibitor prevented lipid damage in the striatum and reduced the levels of protein carbonyl in the hippocampus and striatum. Lipid damage was not reversed by the KMO inhibitor. The KMO inhibitor increased the levels of SOD activity in the hippocampus, and reduced the levels of protein carbonyl while elevating the levels of CAT activity in the striatum of rats that had been injected with ketamine.

    Our findings revealed that the KP pathway could be a potential mechanism by which a schizophrenia animal model induced by ketamine could cause interference by producing behavioral disturbance and inducing oxidative stress in the brain, suggesting that the inhibition of the KP pathway could be a potential target in treating schizophrenia.

    The translocator protein 18 kDa and its role in neuropsychiatric disorders. Translocator protein TSPO is an 18kDa translocator membrane protein expressed in the outer mitochondrial membrane of steroid-synthesizing cells in the central and peripheral nervous systems. TSPO is involved in cellular functions, including the regulation of cell proliferation, transport of cholesterol to the inner mitochondrial membranes of glial cells, regulation of mitochondrial quality control, and haem synthesis.

    In the brain, TSPO has been extensively used as a biomarker of injury and inflammation. Indeed, TSPO was up-regulated in several inflammatory and neurodegenerative diseases. In contrast, the expression of TSPO was decreased in peripheral blood from psychiatric patients. Since TSPO is involved in several mechanisms related to mitochondrial function and inflammatory alterations, therapeutic approaches focusing on the regulation of TSPO may provide a new avenue for the treatment of neuropsychiatric disorders.

    Based on the involvement of mitochondrial alterations in the neurobiology of neuropsychiatric disorders, this review will focus on the functions and physiological roles of TSPO and the potential of TSPO ligands as therapeutic strategies for the treatment of neuropsychiatric disorders. Involvement of the Kynurenine Pathway Modulation.

    Neurological dysfunction as a result of neuroinflammation has been reported in sepsis and cause high mortality. High levels of cytokines stimulate the formation of neurotoxic metabolites by kynurenine KYN pathway. Vitamin B6 vit B6 has anti-inflammatory and antioxidant properties and also acts as a cofactor for enzymes of the KYN pathway.

    Thus, by using a relevant animal model of polymicrobial sepsis, we studied the effect of vit B6 on the KYN pathway, acute neurochemical and neuroinflammatory parameters, and cognitive dysfunction in rats. Twenty-four hours later, the prefrontal cortex and hippocampus were removed for neurochemical and neuroinflammatory analyses. Animals were followed for 10 days to determine survival rate, when cognitive function was assessed by behavioral tests.

    Vitamin B6 interfered in the activation of kynurenine pathway, which led to an improvement in neurochemical and neuroinflammatory parameters and, consequently, in the cognitive functions of septic animals. Thus, the results indicate that vit B6 exerts neuroprotective effects in acute and late consequences after sepsis.

    Early life experience contributes to the developmental programming of depressive-like behaviour, neuroinflammation and oxidative stress. This study used an animal model of depression induced by maternal care deprivation MCD to investigate whether depressive behaviour, neuroinflammation and oxidative stress were underlying factors in developmental programming after early life stress.

    At postnatal days PND 20, 30, 40, and 60, individual subsets of animals were evaluated in behavioural tests and then euthanized to assess cytokine levels and oxidative stress parameters in the prefrontal cortex PFC , hippocampus and serum.

    However, at PND 20 and 60, the rats displayed a depressive-like behaviour in the forced swimming test, without changes in locomotor spontaneous activity.

    Protein carbonyl levels increased in the brain at PND 30, 40 and Superoxide dismutase SOD activity was decreased during all developmental programming phases evaluated in the brain. Our results revealed that "critical episodes" in early life stressful events are able to induce behavioural alterations that persist into adulthood and can stimulate inflammation and oxidative damage in both central and peripheral systems, which are required for distinct patterns of resilience against psychiatric disorders later in life.

    The miRNome of bipolar disorder. Epigenetic mechanisms have been suggested to play a key role in the pathophysiology of bipolar disorder BD , among which microRNAs miRNAs may be of particular significance according to recent studies. We aimed to summarize miRNA studies in BD to identify consistent findings, limitations, and future directions of this emerging field. The included studies report miRNA alterations in postmortem brain tissues and in the periphery, cell culture and preclinical findings, genetic associations, and the effects of medications.

    Several studies report changes in miRNA expression levels in postmortem brain and in the periphery of patients, although most of the results so far have not been replicated and are not concordant between different populations. Genetic studies also suggest that miRNA genes are located within susceptibility loci of BD, and also a putative role of miRNAs in modulating genes previously shown to confer risk of BD. We did not perform a systematic review of the literature, and miRNAs represent only one facet of the plethora of epigenetic mechanisms that might be involved in BD's pathophysiology.

    Accordingly, miRNA might represent important biomarkers of illness to be used in the clinical settings, and potentially also for the development of novel therapeutics for BD in the near future. Methods In the present study, we investigated the effects of Li and TMX on PKC signaling pathway in the frontal cortex and hippocampus of rats submitted to the animal model of mania induced by ouabain.

    We showed that ouabain induced hyperlocomotion in the rats. A possible new target for depression. Depression remains a debilitating condition with an uncertain aetiology. Recently, attention has been given to the renin—angiotensin system.

    In the central nervous system, angiotensin II may be important in multiple pathways related to neurodevelopment and regulation of the stress response. Studies of drugs targeting the renin—angiotensin system have yielded promising results.

    Here, we review the potential beneficial effects of angiotensin blockers in depression and their mechanisms of action. Drugs blocking the angiotensin system have efficacy in several animal models of depression. While no randomised clinical trials were found, case reports and observational studies showed that angiotensin-converting enzyme inhibitors or angiotensin receptor blockers had positive effects on depression, whereas other antihypertensive agents did not. Drugs targeting the renin—angiotensin system act on inflammatory pathways implicated in depression.

    Both preclinical and clinical data suggest that these drugs possess antidepressant properties. In light of these results, angiotensin system-blocking agents offer new horizons in mood disorder treatment. Antimanic activity of minocycline in a GBRinduced model of mania in mice: Possible role of antioxidant and neurotrophic mechanisms. Recently, single administration of the dopamine transporter DAT inhibitor, GBR, was related to mania-like alterations.

    Adult Swiss mice were submitted to 14 days protocols namely prevention and reversal. GBR repeated administration induced hyperlocomotion and increased risk taking behavior that were prevented and reversed by the mood stabilizers and both doses of Mino. Regarding lipid peroxidation Mino was more effective in the prevention and reversal of lipid peroxidation in the hippocampus whereas Li and VAL prevented this alteration in the striatum and PFC.

    GBR repeated administration resembles manic phenotype. Similarly to classical mood-stabilizing agents, Mino prevented and reversed GBR manic-like behavior in mice. Thus, our data provide preclinical support to the design of trials investigating Mino's possible antimanic effects. The different effects of lithium and tamoxifen on memory formation and the levels of neurotrophic factors in the brain of male and female rats.

    Lithium Li is a mood-stabilizing drug used in the treatment of bipolar disorder BD. Recently, preclinical studies have demonstrated the potential of tamoxifen TMX in the treatment of acute episodes of BD. However, the prolonged use of TMX for mood disorders treatment is controversial. In this study, we evaluated the effects of TMX or Li on cognitive behavior, as well as the levels of neurotrophic factors in the brain of male and female rats.

    Male and female Wistar rats received administrations of water control group , TMX or Li via gavage for a period of 28 days; the rats were then subjected to the open-field test to evaluate spontaneous locomotion , and the novel object recognition and step-down inhibitory avoidance tests to evaluate cognition.

    No significant differences were observed in the open-field and inhibitory avoidance tests after drug administration in either the male or female rats. The administration of TMX, but not Li, decreased the recognition index of both the male and female rats in the object recognition test.

    Tamoxifen decreased the levels of NGF in the hippocampus of female rats. In conclusion, it can be suggested that long-term treatments with TMX can lead to significant cognitive impairments by reducing the levels of neurotrophic factors in the brain of rats. Blockade of the angiotensin system improves mental health domain of quality of life: A meta-analysis of randomized clinical trials.

    It is unclear whether blockade of the angiotensin system has effects on mental health. Our objective was to determine the impact of angiotensin converting enzyme inhibitors and angiotensin II type 1 receptor AT1R blockers on mental health domain of quality of life.

    Meta-analysis of published literature. The last search was conducted in January Randomized controlled trials comparing any angiotensin converting enzyme inhibitor or AT1R blocker versus placebo or non-angiotensin converting enzyme inhibitor or non-AT1R blocker were selected. Study participants were adults without any major physical symptoms.

    Eleven studies were included in the analysis. Use of angiotensin blockers and inhibitors for the treatment of hypertension in otherwise healthy adults is associated with improved mental health domains of quality of life. Mental health quality of life was a secondary outcome in the included studies. Research specifically designed to analyse the usefulness of drugs that block the angiotensin system is necessary to properly evaluate this novel psychiatric target. Lithium ameliorates sleep deprivation-induced mania-like behavior, hypothalamic-pituitary-adrenal HPA axis alterations, oxidative stress and elevations of cytokine concentrations in the brain and serum of mice.

    The goal of the present study was to investigate the effects of lithium administration on behavior, oxidative stress parameters and cytokine levels in the periphery and brain of mice subjected to an animal model of mania induced by paradoxical sleep deprivation PSD. Male C57 mice were treated with saline or lithium for 7 days. The sleep deprivation protocol started on the 5th day during for the last 36 hours of the treatment period.

    Immediately after the sleep deprivation protocol, animals locomotor activity was evaluated and serum and brain samples was extracted to evaluation of corticosterone and adrenocorticotropic hormone circulating levels, oxidative stress parameters and citokynes levels. The results showed that PSD induced hyperactivity in mice, which is considered a mania-like behavior. PSD increased lipid peroxidation and oxidative damage to DNA, as well as causing alterations to antioxidant enzymes in the frontal cortex, hippocampus and serum of mice.

    In addition, PSD increased the levels of cytokines in the brains of mice. Treatment with lithium prevented the mania-like behavior, oxidative damage and cytokine alterations induced by PSD.

    Improving our understanding of oxidative damage in biomolecules, antioxidant mechanisms and the inflammatory system - alterations presented in the animal models of mania - is important in helping us to improve our knowledge concerning the pathophysiology of BD, and the mechanisms of action employed by mood stabilizers. Resilience dysregulation in major depressive disorder: Many studies have been shown an important role of glutamatergic system as well microglial activation in the pathophysiology of major depressive disorder MDD.

    Experimental and clinical data suggest that attenuation of N-methyl-D-aspartate NMDA receptor function exerts antidepressant effects. Glutamatergic system is involved with memory establishment and function, and it regulates plasticity in the brain. Microglial cells play pivotal role to the brain functions; however, under chronic inflammation status microglial could be turn activated and increase the pro-inflammatory cytokines.

    In humans most resistant to the development of psychiatric disorders, including MDD, are observed a greater degree of resilience resulting from stress. Less resilience is associated with neuroendocrine and neuroinflammatory markers, as well as with glutamatergic system dysregulation. Thus, this review we highlighted findings from literature identifying the function of glutamatergic system, microglial activation and inflammation in resilience.

    Pathophysiological mechanisms involved in the relationship between diabetes and major depressive disorder. Separately, each presents with several comorbidities for patients.

    These can be seen as proxies of … More. Cannabidiol CBD , one major non-psychotomimetic compound of the cannabis sativa … More. We evaluated cognitive performance in rats that survived from sepsis induced … More. We have studied the effect of training conditions on hippocampal protein synthesis-dependent processes in consolidation of the inhibitory avoidance task.

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    João Quevedo

    JOÃO LUCIANO DE QUEVEDO. The University of Texas I Izquierdo, JA Quillfeldt, MS Zanatta, J Quevedo, E Schaeffer, PK Schmitz, European Journal of. Dr. João Luciano de Quevedo concluded his M.D. in , his residency training in Psychiatry in , his fellowship in Psychopharmacology in and his. In case you missed Dr. João Quevedo's interview about depression, check it out here from the studios of Univision Houston Channel

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    pwner6

    JOÃO LUCIANO DE QUEVEDO. The University of Texas I Izquierdo, JA Quillfeldt, MS Zanatta, J Quevedo, E Schaeffer, PK Schmitz, European Journal of.

    legi147

    Dr. João Luciano de Quevedo concluded his M.D. in , his residency training in Psychiatry in , his fellowship in Psychopharmacology in and his.

    kaktak1111

    In case you missed Dr. João Quevedo's interview about depression, check it out here from the studios of Univision Houston Channel

    marsi

    Phone, Suggest a phone number Consultório Prof. Dr. João Quevedo, Criciúma. 6 likes. Local Business. Dr. João Quevedo. Local Business. Unofficial Page.

    shamon

    Dr. João Luciano de Quevedo is currently Professor of Psychiatry at the McGovern Medical School, The University of Texas Health Science Center at Houston.

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