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Age is associated with increased risk for several disorders including dementias, cardiovascular disease, atherosclerosis, obesity, and diabetes. Age is also associated with cognitive decline particularly in cognitive domains associated with memory and processing speed. With increasing life expectancies in many countries, the number of people experiencing age-associated cognitive impairment is increasing and therefore from both economic and social terms the amelioration or slowing of cognitive aging is an important target for future research. However, the biological causes of age associated cognitive decline are not yet, well understood. In the current review, we outline the role of inflammation in cognitive aging and describe the role of several inflammatory processes, including inflamm-aging, vascular inflammation, and neuroinflammation which have both direct effect on brain function and indirect effects on brain function changes in cardiovascular function.

There is increasing evidence that connections formed between microbiome, the gut, and the brain play a role in health and well-being. Non-pharmaceutical targets for management of mood disorders, such as bipolar disorder, are relatively under-researched. At the same time, it is clear that there is an intimate connection between psychiatry and gastrointestinal health. Here, we have discussed various comorbid conditions associated with bipolar disorders such as inflammation, irritable bowel disease and antibiotic induced mania with importance to demonstrate possible involvement of the gut microbiota. Gut microbiota–targeted preclinical and clinical interventions have demonstrated enhancement in various psychological conditions. Further in this review, we explore links between bipolar disorder, inflammation and gut microbiome with a focus on dietary, pro- and pre-biotic interventions as potential adjuvant therapies for use in the management of mood disorders such as bipolar disorder.

Current literature shows that emotional intelligence (EI) plays a significant role in teacher effectiveness. In recognition of this, one Australian state has recently announced that initial teacher education (ITE) graduates must demonstrate superior emotional intelligence in psychometric tests before they will be allowed to apply for jobs in New South Wales' public schools. In order to inform ITE providers and researchers seeking to support pre-service teachers (PST) in developing superior EI, this scoping review examines what is known from the existing literature about PSTs' EI and identifies gaps in the current literature. There were 23 articles published which fit the criteria for this scoping review, 22 of these used quantitative methods. This scoping review revealed that there is a need for methodological diversification within this field and recommends that future studies focus on qualitative research methods to facilitate in-depth understanding of EI within the context of PST. [Author abstract]

•Hemp-derivative foods often contain trace levels of Δ-9-tetrahydrocannabinol (THC).•A concentration limit of 10mg/kg for hemp-oil is approved for Australia and New Zealand.•The effect of these products on existing drug screening protocols was assessed.•Consumption of hemp-oil does not result in THC-positive oral fluid or blood screens.•10mg/kg imposed limit on THC will not negatively affect local drug screening protocols. Hemp-derivative (Cannabis sativa L.) food products containing trace levels of Δ-9-tetrahydrocannabinol (THC) are proposed for consumption in Australia and New Zealand; however, it is unclear whether use of these products will negatively affect existing drug screening protocols. This double-blind, within-subjects, cross-over trial assessed 35 adults (17 male; 18 female), aged 22–52 years [Mean=30.7, Standard Deviation (S.D)±7.6]. Low dose THC oil [5mL bearer sesame oil containing 10mg/kg THC (0.046mg THC per 5mL dose)]; high dose THC oil [5mL bearer sesame oil containing 20mg/kg THC (0.092mg THC per 5mL dose)]; and a placebo oil (THC negative) was consumed during a three-week protocol. The Securetec Drugwipe® II Twin device assessed THC presence (cut-off 20ng/mL) in oral fluid at baseline, at 5, 30, 60, 120 and 240min post-treatment. Blood was drawn at baseline, 30, 120 and 240min post-treatment, and urine at baseline and 240min post-treatment. No THC was detected in oral fluid, blood or urine samples at any time-point following consumption of the low or high THC dose. Trace concentrations of 11-nor-Δ9-tetrahydrocannabinol-9-carboxylic acid (THCa) were detected in blood 4-h after consumption of the high THC treatment (M=0.0001mg/L) and in urine at 4-h post consumption of both low and high THC treatments (M=0.0001mg/L and 0.0004mg/L, respectively). Consumption of low-content THC oil does not result in positive biological assessments. It is therefore highly unlikely that ingestion of products containing these levels of THC will negatively impact existing region-specific drug driving enforcement protocols.

Background and Objective: With an increase in the number of older citizens in most Western countries, cognitive decline is becoming an increasingly significant issue. Numerous age-related metabolic and physiological changes, such as increased inflammation and oxidative stress, decreased adenosine triphosphate (ATP) production, poorer cardiovascular function, and reduced cerebral blood flow, have been implicated in cognitive decline, prompting research into interventions. Among these, Coenzyme Q10 (CoQ10), an antioxidant and metabolic stimulant, has shown promise in improving some of the underlying biological mechanisms of cognitive decline. However, not much is known about the efficacy of CoQ10 supplementation on cognition in the elderly. Therefore, the aim of this review is to explore the efficacy of CoQ10 supplementation on cognitive function. Methods: We conducted a review of animal studies and human clinical trials investigating the effect of CoQ10 supplementation on cognition in samples who were healthy or with specific diseases. Overall, twelve studies demonstrated improved cognitive function and two showed a reduction in oxidative stress in response to CoQ10 supplementation, either alone or in combination with other compounds. Out of eight human clinical trials in healthy subjects (n = 2) and disease states (n = 6), four showed evidence of a beneficial effect of CoQ10 supplementation on cognition, while two demonstrated an increase in cerebral blood flow. Disparity in the results of the clinical trials presented here is likely due to differing testing procedures, inconsistent use of cognitive assessments, and/or varying bioavailability of different preparations of CoQ10. Conclusions: There is some evidence to suggest that cognition and the biological mechanisms that regulate it are positively impacted by CoQ10 therapy. However, it is crucial to note that the literature presents mixed results, with many human clinical trials also reporting no benefit of CoQ10 supplementation on cognitive performance. To fully evaluate the benefits of CoQ10 on cognitive function in ageing and in neurodegenerative diseases, future studies are needed that target possible mechanisms and utilise a wider range of cognitive assessments.

Brain aging is a complex and multifactorial process broadly involving changes in the brain's structure, neuronal activity, and biochemical profile. These changes in brain function have also been linked to age-associated variations in cognitive function. Recent research has suggested a role of increased oxidative stress and reduced cognition in older people. Therefore, studies that examine the effects of antioxidants on cognitive performance are important, particularly in the context of an increase in elderly populations in most Western countries. One such antioxidant, Pycnogenol, is a standardized plant-based extract obtained from the bark of the French maritime pine and has a long historical use to treat inflammation and improve health. More recently, Pycnogenol has been subjected to more than 100 research trials. and animal studies using the standardized extract have indicated a multimodal action of Pycnogenol, and several human studies have shown improvements in cognitive function after chronic administration. In this paper, we review these studies in the context of understanding both biological and cognitive changes due to Pycnogenol and evaluate possibilities of Pycnogenol to improve neurocognitive function.

RationaleDysregulation of the one carbon cycle is documented in depression. Thereby, S-adenosylmethionine (SAMe), a one–carbon cycle nutraceutical compound with a favourable side effect profile, has a theoretical rationale for efficacy. However, further controlled studies are required to confirm SAMe’s efficacy.ObjectivesTo test the efficacy of SAMe versus placebo in unmedicated DSM-5 diagnosed (major depressive disorder) (MDD) patients with mild-to-moderate levels of depressive symptoms.MethodsWe conducted an 8-week, double-blind, randomised controlled trial testing 800 mg/day of SAMe monotherapy versus placebo in 49 patients with MDD (Montgomery-Åsberg Depression Rating Scale [MADRS] score 14–25) who were not currently taking antidepressants. One–carbon cycle biomarkers, brain-derived neurotropic factor (BDNF), and relevant single nucleotide polymorphisms (SNPs) were analysed as potential treatment moderators.ResultsA clinically relevant differential reduction from baseline to week 8 of 3.76 points occurred on the primary outcome (MADRS) in favour of SAMe. This however was not significant (p = 0.13) on an adjusted linear mixed model, notwithstanding a medium to large effect size of 0.72. A high placebo response rate of 53% occurred (> 50% reduction on MADRS). Exploratory analyses showed that SAMe was however effective in reducing depression amongst participants with milder depression severity (MADRS ≤ 22, p = 0.045). Response was not moderated by BDNF, SNPs, or one–carbon cycle biomarkers, although increased folate concentrations were correlated with improved symptoms in the SAMe group (r = − 0.57, p = 0.026). The treatment was safe and well tolerated.ConclusionsAlthough a differential reduction in depression symptoms between groups was observed in favour of SAMe, the results of this pilot study were not statistically significant.Trial registrationANZCTR—Australian New Zealand Clinical Trials Registry; No.: ACTRN12613001299796; URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=364900

The effects of fish oil (FO) or omega-3 supplementation on cognition has been the subject of several previous clinical trials. However, the effect of different doses taken chronically on cognition in children has not been well studied. In order to address this gap in our knowledge, we conducted a randomized, double-blind, placebo-controlled clinical trial. A total of one hundred and twenty healthy, cognitively normal Thai children aged 6–12 years old consumed daily low dose FO (260 mg Docosahexaenoic acid (DHA)), high dose FO (520 mg DHA), or placebo (Soybean oil) for 12 weeks. Cognitive function was assessed using a computerized cognitive battery, including the Go/NoGo, N-Back, and Digit Span tests as well as concurrent event-related potentials (ERPs), which together measured attention, processing speed, inhibition, and memory at baseline and 12 weeks. We hypothesized that compared to placebo, the two FO groups would show improved cognitive performance and shorter ERP latencies. In total, 42, 39, and 39 participants completed each of the test (FO-A, FO-B) and placebo groups (P) allocations, respectively, and were analyzed (120 in total across the three groups). No significant differences were observed between reaction times (RTs), accuracy, or error rates for all three of the cognitive tests. The ERP measurement and analysis of brain activity during the cognitive tests showed an increase in ERP amplitude. For all cognitive tests, there was a dose-response effect of FO on ERP amplitudes. These findings indicate that fish oil intake leads to a consistent improvement in attention and cognitive processing ability measured by changes in brain activity during working and long-term memory processes. This is the first study to directly quantify such an effect through simultaneous measurement of manual and mental activity during cognitive tasks following chronic FO use in children.

Purpose Depression clinical trials are increasingly studying biomarkers to predict and monitor response to treatment. Assessment of biomarkers may reveal subsets of patients who are responsive to nutraceutical treatment, which may facilitate a personalized approach to treating depression. Methods This is a post hoc analysis of an 8-week, double-blind, randomized, controlled trial ( n  = 158) investigating a combination nutraceutical comprising Omega-3 (EPA 1 g/DHA 656 mg), SAMe, zinc, 5-HTP, folinic acid, and co-factors versus placebo for the treatment of Major Depressive Disorder. The study explored levels of polyunsaturated fatty acids, folate, vitamin B12, zinc, homocysteine, and BDNF as possible predictors and correlates of response to nutraceutical supplementation. Results Concentrations of EPA and DHA in red cell membranes increased in response to treatment and were significantly correlated with a decrease in depressive symptoms during active treatment ( p  = 0.003 and p  = 0.029; respectively). Higher baseline levels of omega-6 fatty acid also correlated with depression reduction in the active treatment group (  p  = 0.011). No other biomarkers were associated with a lessening of depressive symptoms. Conclusion Changes in fatty acid levels resulting from a nutraceutical combination containing EPA and DHA provide a response biomarker in treating depression.

In the current study, sixty healthy older adults aged 50 years or older, and who were light to moderate coffee drinkers, were administered 6g of a decaffeinated green coffee blend (NESCAFÉ Green Blend coffee; GB) or 540mg pure chlorogenic acids (CGA) or placebo in a double-blind acute cross-over design, with cognitive and mood assessments pre-dose, 40-mins and 120-mins post-dose. The primary outcome measure was accuracy in Rapid Visual Information Processing (RVIP). Secondary cognitive outcome measures included RVIP reaction time as well as Inspection time (IT), Jensen Box decision/reaction times, serial subtraction and N-Back working memory. Secondary mood measures included Bond-Lader and caffeine Research visual analogue scales (VAS). No significant treatment effects were found for the primary outcome measure, although significant effects were found amongst secondary measures. Overall, CGA in isolation was not found to significantly improve cognitive function relative to placebo whereas the GB was found to improve sustained attention as measured by the N-Back task in comparison to placebo overall (t=2.45,p=.05), as well as decision time on a 2-choice reaction time task (Jensen box) in comparison to placebo at 40 minutes post-dose (t=2.45,p=.05). Similarly, GB was found to improve alertness on both the Bond-Lader at 120 minutes relative to CGA (t=2.86, p=0.02) and the caffeine Research VAS relative to CGA (t=3.09, p=0.009) and placebo (t=2.75,p=0.02) at 120 minutes post-dose. Both the GB and CGA were also found to significantly improve symptoms of headache at 120 minutes relative to placebo (t=2.51,p=0.03 and t=2.43,p=.04 respectively), whilst there was a trend towards a reduction in jitteriness with GB and CGA in comparison to placebo at 40 minutes post-dose (t=2.24,p=0.06 and t=2.20,p=0.06 respectively). These findings suggest that the improvements in mood observed with GB, but not the improvements in cognitive function, are likely to some extent to be attributable to CGAs. Australia New Zealand Clinical Trials Registry ACTRN12611000067976 www.anzctr.org.au.