New cost-effective psychological interventions are needed to contribute to treatment options for psychiatric and physical health conditions. This systematic review aims to investigate the current literature on one potentially cost-effective form of mindfulness-based therapy, those delivered through technological platforms without any mindfulness facilitator input beyond the initial design of the programme. Three electronic databases (Ovid Medline, PsychINFO and Embase) were searched for relevant keywords, titles, medical subject headings (MeSH) and abstracts using search terms derived from a combination of two subjects: ‘mindfulness’ and ‘technology’. Overall, ten studies were identified. The majority of studies were web-based and similar in structure and content to face-to-face mindfulness-based stress reduction courses. Clinical outcomes of stress (n = 5), depression (n = 6) and anxiety (n = 4) were reported along with mindfulness (n = 4), the supposed mediator of effects. All eight studies that measured significance found at least some significant effects (p < .05). The highest reported effect sizes were large (stress d = 1.57, depression d = .95, both ps > .005). However, methodological issues (e.g. selection bias, lack of control group and follow-up) which reflect the early nature of the work mean these largest effects are likely to be representative of maximal rather than average effects. Whilst there are important differences in the construction, length and delivery of interventions, it is difficult to draw firm conclusions about the most effective models. Suggestions of key characteristics are made though, needing further investigation preferably in standardised interventions. Given the existing research and the speed at which technology is making new platforms and tools available, it seems important that further research explores two parallel lines: first, refinement and thorough evaluation of already established technology-based mindfulness programmes and second, exploration of novel approaches to mindfulness training that combine the latest technological advances with the knowledge and skills of experienced meditation teachers.
The Herb Rhinacanthus nasutus (L.) Kurz, which is native to Thailand and Southeast Asia, has become known for its antioxidant properties. Neuronal loss in a number of diseases including Alzheimer’s disease is thought to result, in part, from oxidative stress. Glutamate causes cell death in the mouse hippocampal cell line, HT-22, by unbalancing redox homeostasis, brought about by a reduction in glutathione levels, and amyloid-β has been shown to induce reactive oxygen species (ROS) production. Here in, we show that ethanol extracts of R. nasutus leaf and root are capable of dose dependently attenuating the neuron cell death caused by both glutamate and amyloid-β treatment. We used free radical scavenging assays to measure the extracts antioxidant activities and as well as quantifying phenolic, flavonoid and sterol content. Molecules found in R. nasutus, lupeol, stigmasterol and β-sitosterol are protective against glutamate toxicity.
Plant parts and their bioactive compounds are widely used by mankind for their health benefits. Cleistocalyx nervosum var. paniala is one berry fruit, native to Thailand, known to exhibit various health benefits in vitro. The present study was focused on analyzing the antiaging, stress resistance, and neuroprotective effects of C. nervosum in model system Caenorhabditis elegans using physiological assays, fluorescent imaging, and qPCR analysis. The results suggest that the fruit extract was able to significantly extend the median and maximum lifespan of the nematode. It could also extend the healthspan by reducing the accumulation of the “age pigment” lipofuscin, inside the nematode along with regulating the expression of col-19, egl-8, egl-30, dgk-1, and goa-1 genes. Further, the extracts upregulated the expression of daf-16 while downregulating the expression of daf-2 and age-1 in wild-type nematodes. Interestingly, it could extend the lifespan in DAF-16 mutants suggesting that the extension of lifespan and healthspan was dependent and independent of DAF-16-mediated pathway. The fruit extract was also observed to reduce the level of Reactive Oxygen Species (ROS) inside the nematode during oxidative stress. The qPCR analysis suggests the involvement of skn-1 and sir-2.1 in initiating stress resistance by activating the antioxidant mechanism. Additionally, the fruit could also elicit neuroprotection as it could extend the median and maximum lifespan of transgenic strain integrated with Aβ. SKN-1 could play a pivotal role in establishing the antiaging, stress resistance, and neuroprotective effect of C. nervosum. Overall, C. nervosum can be used as a nutraceutical in the food industry which could offer potential health benefits.
Alzheimer's disease is a neurodegenerative disease that affects 44 million people worldwide, costing the world $605 billion to care for those affected not taking into account the physical and psychological costs for those who care for Alzheimer's patients. Dipentylammonium is a simple amine, which is structurally similar to a number of other identified sigma-1 receptor ligands with high affinities such as (2R-trans)-2butyl-5-heptylpyrrolidine, stearylamine and dodecylamine. This study investigates whether dipentylammonium is able to provide neuroprotective effects similar to those of sigma-1 receptor agonists such as PRE-084. Here we identify dipentylammonium as a sigma-1 receptor ligand with nanomolar affinity. We have found that micromolar concentrations of dipentylammonium protect from glutamate toxicity and prevent NFκB activation in HT-22 cells. Micromolar concentrations of dipentylammonium also protect stably expressing amyloid precursor protein Swedish mutant (APP/Swe) Neuro2A cells from toxicity induced by 150 μM dopamine, suggesting that dipentylammonium may be useful for the treatment of Parkinsonian symptoms in Alzheimer's patients which are often associated with a more rapid deterioration of cognitive and physical ability. Finally, we found that low micromolar concentrations of dipentylammonium could out preform known sigma-1 receptor agonist PRE-084 in potentiating neurite outgrowth in Neuro2A cells, further suggesting that dipentylammonium has a potential use in the treatment of neurodegenerative diseases and could be acting through the sigma-1 receptor.
BACKGROUND AND PURPOSESigma-1 receptors are atypical receptors with potentially two transmembrane domains. Antagonists require doses significantly higher than their published affinities to have biological effects. We have reassessed the binding characteristics of these ligands and found antagonists bind to high-and low-affinity states not distinguished by agonists. EXPERIMENTAL APPROACHThe affinities of sigma-1 receptor ligands was assessed using radioligand saturation and competition binding of [ 3 H]-(+)-pentazocine to permeabilized MDA-MB-468 cells. This was compared with the effect of ligands on metabolic activity using an MTS-based assay and calcium signalling using cells loaded with the calcium dye, Fura-2. KEY RESULTSSigma-1 receptor antagonists, but not agonists, show GTP-and suramin-sensitive high-affinity binding. Functional responses (calcium signalling and metabolic activity), while associated with sigma-1 receptor binding, required binding to an unidentified, low-affinity target. CONCLUSIONS AND IMPLICATIONSSigma-1 receptors are coupled to G proteins. This interaction is only observed when analysing antagonist binding. The identity of the G protein remains to be resolved. The concept of agonist and antagonist at the sigma-1 receptor needs to be revisited. Abbreviations(+)-3-PPP, (+)-3-(3-hydroxyphenyl)-N-1-(propyl)piperidine; [Ca 2+ ], free concentration of Ca 2+ ions; DMT, N,Ndimethyltryptamine; IPAG, 1-(4-iodophenyl)-3-(2-adamantyl)guanidine; SKF-10047, N-allylnormetazocine IntroductionThe search for understanding of the sigma-1 receptor has been a long, mysterious and as yet incomplete journey. The receptor has mostly been studied within the CNS. However, more recent work over the past decade has shown the receptor to be abundant in neuronal, and non-neuronal tissues (Vilner et al., 1995) leading to its study in cancer biology (Spruce et al., 2004).The sigma receptor was proposed as a novel fourth opioid receptor in 1976 to account for the behavioural effects of N-allylnormetazocine (SKF-10047), which could not be accounted for by the m (morphine) or k (ketocyclazocine) receptors (Martin et al., 1976). SKF-10047 was defined as an agonist as it raised pulse and respiration rates, as well as body temperature and caused dilatation of pupils in beagles. Interestingly, m-receptor agonists lowered pulse and respiration rates, as well as body temperature and produced classic BJP British Journal of Pharmacology DOI:10.1111DOI:10. /j.1476DOI:10. -5381.2011 772 British Journal of Pharmacology (2011) 164 772-780The Authors British Journal of Pharmacology © 2011 The British Pharmacological Society pinpoint pupils. Sigma-1 receptor antagonists were defined as agents that were able to prevent these responses. Later studies (e.g. Spruce et al., 2004) suggested that biochemically, agonists do not cause activation of the receptor but can block the effects of antagonists which do. More recently, data obtained using mice in which the sigma-1 receptor has been knocked out further cloud the picture; expression o...
Rhinacanthus nasutus (L.) Kurz (Acanthaceae) is an herb native to Thailand and Southeast Asia, known for its antioxidant properties. Hypoxia leads to an increase in reactive oxygen species in cells and is a leading cause of neuronal damage. Cell death caused by hypoxia has been linked with a number of neurodegenerative diseases including some forms of dementia and stroke, as well as the build up of reactive oxygen species which can lead to diseases such as Huntington’s disease, Parkinson’s disease and Alzeheimer’s disease. In this study we used an airtight culture container and the Mitsubishi Gas Company anaeropack along with the MTT assay, LDH assay and the trypan blue exlusion assay to show that 1 and 10 µg mL−1 root extract of R. nasutus is able to significantly prevent the death of HT-22 cells subjected to hypoxic conditions, and 0.1 to 10 µg mL−1 had no toxic effect on HT-22 under normal conditions, whereas 100 µg mL−1 reduced HT-22 cell proliferation. We also used H2DCFDA staining to show R. nasutus can reduce reactive oxygen species production in HT-22 cells.
Neurodegenerative disease is a collective term given for the clinical condition, which results in progressive degeneration of neurons and the loss of functions associated with the affected brain region. Apart from the increase in age, neurodegenerative diseases are also partly affected by diet and lifestyle practices. Parkinson’s disease (PD) is a slow onset neurodegenerative disorder and the second most common neurodegenerative disease, which affects the motor system. Although there is no prescribed treatment method to prevent and cure PD, clinical procedures help manage the disease symptoms. Green tea polyphenols are known for several health benefits, including antioxidant, anti-inflammatory, and neuroprotective activity. The current manuscript summarizes the possible mechanisms of neuroprotective potential of green tea with a special focus on PD. Studies have suggested that the consumption of green tea protects against free-radicals, inflammation, and neuro-damages. Several in vivo studies aid in understanding the overall mechanism of green tea. However, the same dose may not be sufficient in humans to elicit similar effects due to complex physiological, social, and cultural development. Future research focused on more clinical trials could identify an optimum dose that could impart maximum health benefits to impart neuroprotection in PD.
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