Blood pressure mediated the effects of cognitive function impairment related to aluminum exposure in Chinese aluminum smelting workers.

OBJECTIVES: The aim of this study is to investigate the effects that the Al on blood pressure and the effect of hypertension in aluminum-induced cognitive impairment in electrolytic aluminum worker. METHODS: The study was conducted 392 male aluminum electrolytic workers in an aluminum plant of China. The concentration of alumina dust in the air of the electrolytic aluminum workshop is 1.07 mg/m3-2.13 mg/m3. According to the Permissible concentration-Time Weighted Average of alumina dust is 4 mg/m3, which does not exceed the standard. The blood pressure of the workers was measured. The plasma aluminum concentration of workers was determined by ICP-MS (Inductively Coupled Plasma Mass Spectrometry). Cognitive functions were measured using MMSE (Mini-Mental State Examination), VFT (Verbal Fluency Test), ATIME (Average Reaction Time), FOM (Fuld Object Memory Evaluation), DST (Digit Span Test), CDT (Clock Drawing Test) scales. Modified Poisson regression was used to analyze the risk of hypertension and cognitive impairment with different plasma aluminum concentrations. Generalized linear regression model was used to analyze the relationship between aluminum and cognitive function, blood pressure and cognitive function. Causal Mediation Analysis was used to analyze the mediation effect of blood press in aluminum-induced cognitive impairment. RESULTS: Plasma aluminum appeared to be a risk factor for hypertension (PR (prevalence ratio) = 1.630, 95 %-CI (confidence interval): 1.103-2.407), systolic blood pressure (PR = 1.578, 95 %-CI: 1.038-2.399) and diastolic blood pressure (PR = 1.842, 95 %-CI: 1.153-2.944). And plasma aluminum increased by e-fold, the scores of MMSE and VFT decreased by 0.630 and 2.231 units respectively and the time of ATIME increased by 0.029 units. In addition, generalized linear regression model showed that blood press was negatively correlated with the scores of MMSE and VFT. Finally, causal Mediation Analysis showed that hypertension was a part of the mediating factors of aluminum-induced decline in MMSE score, and the mediating effects was 16.300 % (7.100 %, 33.200 %). In addition, hypertension was a part of the mediating factors of aluminum-induced decline in VFT score, and the mediating effects was 9.400 % (2.600 %, 29.000 %) CONCLUSION: Occupational aluminum exposure increases the risk of hypertension and cognitive impairment. And hypertension may be a mediating factor of cognitive impairment caused by aluminum exposure.

Olive oil and oleic acid-based self nano-emulsifying formulation of omega-3-fatty acids with improved strength, stability, and therapeutics.

AIM: To develop, characterise, and optimise SNEDDS formulation to enhance organoleptics, bioavailability, physical & oxidative-stability, and extend shelf-life of pure Ω-3-fatty acids oil for use in the food fortification industry as nutraceuticals. METHODS: SNEDDS formulations were prepared using a simple stirring technique and optimised based on in-vitro characterisation. RESULTS: The optimised SNEDDS formulation (F3) had a mean diameter of 52.9 ± 0.4 nm, PDI of 0.229 ± 0.02, zeta potential of -17.3 ± 0.1 mV, cloud temperature of 92 ± 0.2 °C, self-emulsification time of 50 ± 0.2 sec, and stable under accelerated stability conditions. Intestinal permeability study on rat ileum depicted absorption of 88.5 ± 0.2% DHA at 5 h for F3 formulation in comparison to 61.5 ± 0.2% for commercial counterpart. F3 formulation exhibited better therapeutics for melamine-induced cognitive dysfunction. CONCLUSIONS: The developed Ω-3-loaded SNEDDS heralds the future for an efficacious, safer, and higher strength formulation intended as a better substitute for currently available formulations.

Neuroprotective effect of hesperidin against emamectin benzoate-induced neurobehavioral toxicity in rats.

Emamectin Benzoate (EMB) is an avermectin insecticide widely used in agriculture and veterinary medicine. Hesperidin (HSP) is a flavanone glycoside predominantly found in citrus fruits and has various beneficial health effects. The current research was conducted to study the neurobehavioral toxic effects of EMB in rats and also to evaluate the protective effect of HSP against these toxic effects. Sixty Sprague-Dawley rats were randomly divided into 4 equal groups: control group, EMB group, HSP group, and EMB + HSP group. EMB (8.8. mg/kg) and/or HSP (100 mg/kg) were administered daily by gavage for 8 weeks. The behavioral assessment demonstrated the adverse effects of EMB on the behavioral, motor, and cognitive brain functions. Exposure to EMB also decreased the activity of antioxidants (catalase and reduced glutathione) and increased the malondialdehyde level in nervous tissue. Moreover, EMB increased the level of inflammatory cytokines (tumor necrosis factor-α and interleukin-1ß) and decreased brain-derived neurotrophic factor (BDNF) levels in rats' brains. On the other hand, concurrent administration of HSP ameliorated the toxic effects of EMB as indicated by improvements in neural functions and reduction of oxidative stress and inflammation. The study concluded that exposure to EMB induces toxic effects in the brain of rats and that HSP has a protective effect against these toxic effects.

Lavender and coriander essential oils and their main component linalool exert a protective effect against amyloid-ß neurotoxicity.

Alzheimer's disease (AD) is a neurodegenerative disorder leading to cognitive deficits and cognitive decline. Since no cure or preventing therapy is currently available to counteract AD, natural-derived compounds are investigated to find new potential neuroprotective agents for its treatment. In the present study, we tested the neuroprotective effect of lavender and coriander essential oils (EOs) and their main active constituent linalool, against the neurotoxicity elicited by Aß1-42 oligomers, a key molecular factor in the neurodegeneration of AD. Importantly, our findings on neuronally differentiated PC12 cells exposed to Aß1-42 oligomers are in accordance with previous in vivo studies reporting the neuroprotective potential of lavender and coriander EOs and linalool. We found that lavender and coriander EOs at the concentration of 10 µg/mL as well as linalool at the same concentration were able to improve viability and to reduce nuclear morphological abnormalities in cells treated with Aß1-42 oligomers for 24 hours. Lavender and coriander EOs and linalool also showed to counteract the increase of intracellular reactive oxygen species production and the activation of the pro-apoptotic enzyme caspase-3 induced by Aß1-42 oligomers. Our findings provide further evidence that these EOs and their main constituent linalool could be natural agents of therapeutic interest against Aß1-42 -induced neurotoxicity.

Involvement of Oxidative Stress and Nerve Growth Factor in Behavioral and Biochemical Deficits of Experimentally Induced Musculoskeletal Pain in Mice: Ameliorative Effects of Heraclin.

Musculoskeletal pain is a widespread complex regional pain syndrome associated with altered emotional and cognitive functioning along with heightened physical disability that has become a global health concern. Effective management of this disorder and associated disabilities includes accurate diagnosis of its biomarkers and instituting mechanism-based therapeutic interventions. Herein, we explored the role of heraclin, a plant-derived molecule, in musculoskeletal pain and its underlying mechanistic approaches in an experimental mouse model. Reserpine (0.5 mg/kg) for 3 consecutive days evoked hyperalgesia, motor incoordination, lack of exploratory behavior, anxiety, and cognition lapse in mice. Reserpine-challenged mice displayed higher serum cytokine level, altered brain neurotransmitter content, elevated brain and muscle oxidative stress, and upregulated brain nerve growth factor receptor expression. Treatment with heraclin (10 mg/kg for 5 consecutive days) exerted analgesic effect and improved motor coordination and memory deficits in mice. Heraclin arrested serum cytokine rise, normalized brain neurotransmitter content, reduced tissue oxidative stress, and downregulated the nerve growth factor receptor expression. Therefore, it may be suggested that heraclin exerts beneficial effects against reserpine-induced musculoskeletal pain disorder possibly through the attenuation of NGFR-mediated pain and inflammatory signaling. Graphical Abstract.

Pubertal fenvalerate exposure impairs cognitive and behavioral development partially through down-regulating hippocampal thyroid hormone receptor signaling.

Fenvalerate, a synthetic pyrethroid insecticide, is an environmental endocrine disruptor and neurodevelopmental toxicant. An early report found that pubertal exposure to high-dose fenvalerate impaired cognitive and behavioral development. Here, we aimed to further investigate the effect of pubertal exposure to low-dose fenvalerate on cognitive and behavioral development. Mice were orally administered with fenvalerate (0.2, 1.0 and 5.0 mg/kg) daily from postnatal day (PND) 28 to PND56. Learning and memory were assessed by Morris water maze. Anxiety-related activities were detected by open-field and elevated plus-maze. Increased anxiety activities were observed only in females exposed to fenvalerate. Spatial learning and memory were damaged only in females exposed to fenvalerate. Histopathology observed numerous scattered shrinking neurons and nuclear pyknosis in hippocampal CA1 region. Neuronal density was reduced in hippocampal CA1 region of fenvalerate-exposed mice. Mechanistically, hippocampal thyroid hormone receptor (TR)ß1 was down-regulated in a dose-dependent manner in females. In addition, TRα1 was declined only in females exposed to 5.0 mg/kg fenvalerate. Taken together, these suggests that pubertal exposure to low-dose fenvalerate impairs cognitive and behavioral development in a gender-dependent manner. Hippocampal TR signaling may be, at least partially, involved in fenvalerate-induced impairment of cognitive and behavioral development.

Cardiotoxicity of doxorubicin-based cancer treatment: What is the protective cognition that phytochemicals provide us?

Doxorubicin (DOX) continues to attract the interest of preclinical and clinical investigations despite its longer-than-50-year record of longevity. The clinical application of DOX can be regarded as a sort of double-edged sword. On one hand, anthracyclines play an indisputable key role in the treatment of tumors; on the other hand, their chronic administration leads to cardiomyopathy and congestive heart failure, which is usually refractory to common medications. Finding the ideal cardioprotective agents has always been the focus of oncologists and cardiologists. Researchers put a lot of energy into phytochemicals because they are often in line with the expected standards, that is, to improve DOX-induced cardiotoxicity without compromising the clinical efficacy or to even produce synergy. We summarized the previous efforts, briefly outlined the mechanism of DOX cardiotoxicity, and focused on exploring the protective effects and potential mechanisms of all phytochemical types that have been investigated under DOX-induced cardiotoxicity. Phytochemicals have been found to be potential cardioprotective agents with universal safety and effectiveness. As a resource repository of pharmacophores, phytochemicals deserve to be utilized as drug templates for further development and research in combating DOX-induced cardiotoxicity.

Study of efficacy and safety of Jiaotai pill in the treatment of depression.

BACKGROUND: Depression is a common affective disorder characterized by marked and lasting melancholia, with corresponding thought and behavior changes. Due to an accelerated pace of life and increased work pressure, the incidence of depression has risen sharply, causing great harm to family and social life. Jiaotai pill (JTP) is a Chinese herbal formula that is commonly prescribed for depression and insomnia in clinical treatment, and exhibits antidepressant effects as shown in animal experimental research. However, there are no standard clinical trials to confirm its efficacy in treating depression. OBJECTIVE: This study aims to assess the efficacy and safety of JTP in the treatment of depression, so as to tap the clinical efficacy advantages of JTP and provide data support for its clinical application. METHODS: A randomized, multicenter clinical trial with parallel groups was designed in this study. A total of 40 patients with depression were included and randomly divided to either the treatment or the control group with a ratio of 1:1. The patients received JTP plus fluoxetine or fluoxetine alone once per day for 8 weeks. The primary outcome included the Hamilton Depression Rating Scale score for patients and brain structure and function by functional magnetic resonance imaging. The secondary outcomes included Traditional Chinese medicine syndrome integral scale scores, Wisconsin Card Sorting Test, blood metabonomics, urine metabonomics. CONCLUSION: The results of this trial will find changes in brain structure, brain function, and metabolism in patients with depression, and provide critical evidence for JTP in the treatment of depression.

Butanol Extract of Tinospora cordifolia Ameliorates Cognitive Deficits Associated with Glutamate-Induced Excitotoxicity: A Mechanistic Study Using Hippocampal Neurons.

Overstimulation of glutamate receptors leads to development of excitotoxicity, which is implicated as final destructive pathway in neurodegenerative diseases. Development of alternative therapeutic strategies effective against glutamate-induced excitotoxicity is much in demand. Herbal drug development is emerging as a major research area for the treatment of various debilitating diseases due to multimodal action and least side effects of herbal products. The current study was aimed to investigate neuroprotective potential of butanol extract of Tinospora cordifolia (B-TCE) against glutamate-induced excitotoxicity using primary hippocampal neurons as in vitro and Wistar strain albino rats as in vivo model systems. Molecular and behavioral parameters were studied to elucidate the underlying mechanism of beneficial effects of B-TCE. B-TCE treatment was also effective in prevention of anxiety, cognition, and motor-coordination deficits induced by glutamate. B-TCE pre-treatment protected the hippocampal neurons from glutamate-induced neurodegeneration and impaired plasticity. At molecular level, B-TCE was observed to attenuate overactivation of glutamate receptors. B-TCE promoted upregulation of ERK and AKT pathways of synaptic plasticity and cell survival in the hippocampus region of brain. This study provides first evidence of neuroprotective potential of B-TCE against glutamate-induced excitotoxicity in hippocampus region and suggests that B-TCE may act as a potential candidate for neuroprotective therapeutic approaches. A single compound 'tinosporicide' was further isolated from B-TCE, which was found to be effective at 800× lower concentration against glutamate-induced neurodegeneration under in vitro conditions.

Verapamil attenuates scopolamine induced cognitive deficits by averting oxidative stress and mitochondrial injury - A potential therapeutic agent for Alzheimer's Disease.

Alzheimer's disease (AD) is a multifactorial disorder where amyloid beta (Aß) plaques, Ca2+ dysregulation, excessive oxidative stress, mitochondrial dysfunction and synaptic loss operate synergistically to bring about cholinergic deficits and dementia. New therapeutic interventions are gaining prominence as the morbidity and mortality of AD increases exponentially every year. Treating AD with antihypertensive drugs is thought to be a promising intervention; however, its mechanism of action of ameliorating AD needs further investigation. In this context, the present study explores the protective effect of verapamil, an antihypertensive agent of Ca2+ channel blocker (CCB) class against scopolamine-induced in vitro neurotoxicity and in vivo cognitive impairment. Supplementation of verapamil was found to attenuate oxidative stress by preventing mitochondrial injury, and augment the expression of genes involved in the cholinergic function (mACR1), synaptic plasticity (GAP43, SYP) and Ca2+-dependent memory-related genes (CREB1, CREBBP, BDNF). Further, verapamil treatment in mice attenuated the cognitive and behavioural deficits induced by scopolamine as measured by the elevated plus maze and passive avoidance test (P < 0.05). Thus, the present study demonstrates the neuroprotective effect of verapamil against the pathogenesis of AD such as oxidative stress, mitochondrial dysfunction and cognitive decline. These observations emphasize the importance of ?Ca2+ dysregulation' and ?mitochondrial dysfunction' theories in AD and recommends the supplementation of compounds that regulate Ca2+ homeostasis and mitochondrial function in susceptible AD individuals.

1-Methylnicotinamide attenuates lipopolysaccharide-induced cognitive deficits via targeting neuroinflammation and neuronal apoptosis.

Alzheimer's disease (AD) is a neurodegenerative disease that affects cognition and behavior. The neuroinflammatory response in the brain is an important pathological characteristic in AD. In this study, we investigated the neuroprotective effects of 1-Methylnicotinamide (MNA), known as the main metabolite of nicotinamide, on reducing lipopolysaccharide (LPS)-induced cognitive deficits via targeting neuroinflammation and neuronal apoptosis. We found that the mice treated with LPS exhibited cognitive deficits in the novel object recognition, Morris water maze and Y-maze avoidance tests. However, intragastric administration of MNA (100 or 200 mg/kg) for 3 weeks significantly attenuated LPS-induced cognitive deficits in mice. Importantly, MNA treatment suppressed the protein expression of nuclear factor-kappa B p65 (NF-κB p65), pro-inflammatory cytokines (TNF-α, IL-6) and decreased the activation of microglia and astrocytes in the hippocampus and frontal cortex of LPS-induced mice. In addition, MNA treatment suppressed neuronal apoptosis by reducing the number of TUNEL-positive cells, caspase-3 activation and increasing the level of Bcl-2/Bax ratio in the hippocampus and frontal cortex. These findings indicate that MNA could be a potential neuroprotective drug in neurodegenerative diseases such as AD.

Individualized Piano Instruction for Improving Cognition in Breast Cancer Survivors.

PURPOSE: To evaluate the use of individualized piano instruction (IPI) for improving cognition among breast cancer survivors. PARTICIPANTS & SETTING: Six participants were included in an eight-week piano program with three data collection time points at baseline, midpoint, and postintervention. Participants were recruited from the breast cancer clinic of a university cancer center in South Florida. METHODOLOGIC APPROACH: Neurocognitive, psychosocial, and self-report assessments were conducted to determine potential benefits and program feasibility, including the NIH Toolbox® Cognition Battery, the Functional Assessment of Cancer Therapy (FACT)-Cognitive Function, the FACT-Breast, the Patient Health Questionnaire-9, the Generalized Anxiety Disorder-7, and a participant questionnaire. FINDINGS: Results related to potential benefits suggest that IPI may significantly improve overall cognition in breast cancer survivors, with fluid cognition showing improvement. In addition, IPI may improve quality of life and self-reported measures of depression and anxiety, with large to moderate effect sizes, respectively. IMPLICATIONS FOR NURSING: Nurses should explore different treatment options for chemotherapy-related cognitive impairment and consider including IPI in survivorship care plans.

Neuroprotective Potential of Curcumin-Loaded Nanostructured Lipid Carrier in an Animal Model of Alzheimer's Disease: Behavioral and Biochemical Evidence.

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases and is caused by accumulation of amyloid-ß (Aß) peptide and is associated with neurological abnormalities in learning and memory. The protective role of curcumin on nerve cells, along with a potent antioxidant and free radical scavenging activity, has been widely studied. However, its low bioavailability and limited transport ability across the blood-brain barrier are two major drawbacks of its application in the treatment of different neurodegenerative diseases. The present study was designed to improve the effectiveness of curcumin in the treatment of Aß-induced cognitive deficiencies in a rat model of AD by loading it into nanostructured lipid carriers (NLCs). The accumulation rate of curcumin (505.76±38.4 ng/g-1 h) in rat brain, as well as its serum levels, were significantly increased by using curcumin-loaded NLCs. The effective role of NLCs for brain delivery of curcumin was confirmed by reduced oxidative stress parameters (ROS formation, lipid peroxidation, and ADP/ATP ratio) in the hippocampal tissue and improvement of spatial memory. Also, histopathological studies revealed the potential of Cur-NLCs in decreasing the hallmarks of Aß in AD in the animal model. The result of studying the neuroprotective potential of Cur-NLC in both pre-treatment and treatment modes showed that loading curcumin in NLCs is an effective strategy for increasing curcumin delivery to the brain and reducing Aß-induced neurological abnormalities and memory defects and that it can be the basis for further studies in the area of AD prevention and treatment.

Neuroprotective effects of Withania somnifera in BPA induced-cognitive dysfunction and oxidative stress in mice.

BACKGROUND: Bisphenol A (BPA), a major endocrine disruptor and a xenobiotic compound is used abundantly in the production of polycarbonate plastics and epoxy resins. Human exposure to this compound is primarily via its leaching from the protective internal epoxy resin coatings of containers into the food and beverages. In addition, the plastics used in dental prostheses and sealants also contain considerable amount of BPA and have a high risk of human exposure. Since it is a well-known endocrine disruptor and closely mimics the molecular structure of human estrogen thereby impairing learning and memory. Withania somnifera (Ws), commonly known as Ashwagandha is known for its varied therapeutic uses in Ayurvedic system of medicine. The present study was undertaken to demonstrate the impairment induced by BPA on the spatial learning, working memory and its alleviation by Ws in Swiss albino mice. The study was conducted on thirty Swiss albino mice, randomly distributed among three groups: control, BPA and BPA + Ws. The behavioral recovery after treatment with Ws was investigated using the Y-maize and Morris water maize test. Whereas, for the estimation of recovery of NMDA receptor which is related to learning and memory in hippocampus region by western blot and immunohistochemistry. Furthermore, the oxidative stress and antioxidant level was assessed by biochemical tests like MDA, SOD and catalase. RESULTS: The study revealed that administration of Ws alleviated the behavioral deficits induced by BPA. Alongside, Ws treatment reinstated the number of NMDA receptors in hippocampus region and showed anti-oxidative property while ameliorating the endogenous anti-oxidant level in the brain. CONCLUSION: These findings suggest that Ws significantly ameliorates the level of BPA intoxicated oxidative stress thereby potentially treating cognitive dysfunction which acts as the primary symptom in a number of neurodegenerative diseases.

Combination of chick embryo and nutrient mixture prevent D-galactose-induced cognitive deficits, immune impairment and oxidative stress in aging rat model.

Aging is spontaneous and inevitable processes that lead to changes in biological systems. The present paper was designed to investigate the anti-aging roles of chick embryo (CE) and nutrient mixture (NM) in aging rats. Aging was induced by administration of D-galactose (D-gal, 500 mg/kg/day for 90 days). CE and NM were administered to aging rats through different dose gavage once a day. Cognitive function assessment was performed using the Morris water maze test. At the end of experiment, serum and tissues were collected for immunity and antioxidation function. The organs and tissues were excised for histological study. The results demonstrated that CE plus NM was superior treatment to improve the histopathologic changes and reverse learning and memory impairment of the aging rats. CE plus NM also increased the spleen and thymus index as well as splenocyte proliferation, and reversed inflammatory cytokine levels. In addition, the biochemical index showed that CE plus NM could improve the antioxidant enzyme activity of the aging rats, decrease lipofuscin (LF) and glutamate content. CE plus NM also inhibited the activation of TLR4/NF-κB pathway stimulated by LPS in splenic B lymphocytes. Overall, these results seem to be implying that CE plus NM was used as potentially natural supplement or functional food for preventing aging.

Protective Effects of 1-Methylnicotinamide on Aß1-42-Induced Cognitive Deficits, Neuroinflammation and Apoptosis in Mice.

The neurotoxicity of Aß peptides has been well documented, but effective neuroprotective approaches against Aß neurotoxicity are unavailable. In the present study, we investigated effects of 1-Methylnicotinamide (MNA), known as a main metabolite of nicotinamide (NA), on the impairment of learning and memory induced by Aß and the underlying mechanisms. We found that intragastric administration of MNA at 100 or 200 mg/kg for 3 weeks significantly reversed bilateral intrahippocampal injection of Aß1-42-induced cognitive impairments in the Morris water maze (MWM), Y-maze and Novel object recognition tests. Furthermore, MNA suppressed Aß1-42-induced neuroinflammation, characterized by suppressed activation of microglia, decreased the expression of IL-6, TNF-α and nuclear translocation of NF-κB p65, as well as attenuated neuronal apoptosis as indicated by decreased TUNEL-positive cells and ratio of caspase-3 fragment to procaspase-3, and increased ratio of Bcl-2/Bax in the hippocampus. Our results show that MNA may ameliorate Aß1-42-induced cognition deficits, which is involved in inhibition of neuroinflammation and apoptosis mediated by NF-κB signaling, suggesting that MNA could have potential therapeutic value for AD. Graphical Abstract Neuroprotective affect of MNA on Aß1-42-induced cognitive deficits.

Cerebrosides from Sea Cucumber Improved Aß1-42 -Induced Cognitive Deficiency in a Rat Model of Alzheimer's Disease.

SCOPE: Cerebrosides are a class of neutral glycosphingolipids, which are widely found to be present in brain tissue. In this study, the protective effect of sea cucumber cerebrosides (Cer) against ß-amyloid (Aß)-induced cognitive impairment is investigated. METHODS AND RESULTS: Male SD rats receive a ventricle injection Aß1-42 peptide to establish an Alzheimer's disease model. Then, the protective effects of Cer against Aß1-42 -induced cognitive impairment by gavage and feed addition are evaluated. The Morris water maze test results show that oral administration of Cer can significantly ameliorate Aß1-42 -induced cognitive deficiency at both high dose (200 mg per kg·per day) and low dose (40 mg per kg·per day) for 27 days. Dietary supplement of Cer by feed addition also exhibits the amelioration on the impaired cognitive function. Further findings indicate that Cer ameliorates Aß1-42 -induced neuronal damage and suppresses the induced apoptosis by decreasing the level of Bax/Bcl-2. Additionally, Cer enhances the expressions of PSD-95 and synaptophysin by activating BDNF/TrkB/CREB signaling pathway, thereby ameliorating Aß1-42 -induced synaptic dysfunction. Furthermore, Cer attenuates Aß1-42 -induced tau hyperphosphorylation by activating the PI3K/Akt/GSK3ß signaling pathway. CONCLUSION: Sea cucumber cerebrosides possess neuroprotective effects against Aß1-42 -triggered cognitive deficits, which may be a potential nutritional preventive strategy for neurodegenerative diseases.

[Management of side effects related to adjuvant hormone therapy in young women with breast cancer]. / Gestion des effets secondaires de l'hormonothérapie du cancer du sein chez la femme jeune.

Despite proven survival benefits after breast cancer, long-trem compliance with adjuvant hormone therapy remains a major issue, partly due to the side effects of treatment. In young women treated for breast cancer, these treatments include tamoxifen, anti-aromatase and LH-RH analogues, with even more side effects when these treatments are combined, especially for younger patients with more aggressive disease. The management of the potential side effects requires first of all detailed and precise information at initiation of treatment, and preventive measures including patient education. Once the treatment has been initiated, clinicians should be able to propose to their patients appropriate measures to alleviate the potential of the side effects, which can be of various types: biological (dyslipidemia), physical (weight gain, hot flushes, vaginal dryness, sexual disorders with low libido, musculoskeletal symptoms…) or psychosocial (anxio-depressive disorders, poor body image, difficulties of professional reintegration). Management of these effects can combine various modalities: drugs (switching hormone therapy, anti-depressants, hormonal treatments of vaginal dryness in some cases, gabapentin), physical treatments (CO2 laser for vulvovaginal atrophy) or psycho-physical techniques (physical activity, mindfulness, acupuncture…). Eventually, the lenghth of these adjuvant hormonal treatments requires supportive measures to help young patients engage in new lifestyle measures, in particular in term of physical activity and diet. This will help them mitigate the symptoms related to these side-effects while reducing the long-term risks related to their disease and treatments.

Reversal of reserpine-induced depression and cognitive disorder in zebrafish by sertraline and Traditional Chinese Medicine (TCM).

BACKGROUND: With increased social pressure, individuals face a high risk of depression. Subsequently, depression affects cognitive behaviour and negatively impacts daily life. Fortunately, the Traditional Chinese Medicine Jia Wei Xiao Yao (JWXY) capsule is effective in reducing depression and improving cognitive behaviour. METHODS: The constituents of JWXY capsule were identified by ultra-performance liquid chromatography and quadrupole time-of-flight mass spectrometry analyses. We analysed behaviours of depression-like zebrafish in the novel tank with an automatic 3D video-tracking system and conducted the colour preference test, as well detected physiological changes after sertraline and JWXY capsule treatments. RESULTS: Both sertraline and JWXY capsule rescued the decreased locomotive behaviour and depression phenotype of zebrafish caused by reserpine. JWXY capsule especially improved the inhibited exploratory behaviour caused by reserpine. In addition, with the onset of depressive behaviour, zebrafish exhibited alterations in cognitive behaviour as indicated by colour preference changes. However, compared with sertraline, JWXY capsule was more efficaciously in rescuing this change in the colour preference pattern. Moreover, an increased level of cortisol, increased expression of tyrosine hydroxylase (TH) and decreased monoamine neurotransmitters, including serotonin (5-HT) and noradrenaline, were involved in the depressive behaviours. In addition, sertraline and JWXY capsule rescued the depressive phenotype and cognitive behaviour of zebrafish by altering the levels of endogenous cortisol and monoamine neurotransmitters. CONCLUSIONS: JWXY capsule was more effectively than sertraline in rescuing reserpine-induced depression and cognitive disorder in zebrafish. Potentially, our study can provide new insights into the clinical treatment of depression and the mechanism of action of JWXY capsule.

Effect of integrated yoga on anti-psychotic induced side effects and cognitive functions in patients suffering from schizophrenia.

Background Twenty one (12 females) subjects, diagnosed with schizophrenia by a psychiatrist using ICD-10, in the ages 52.87 + 9.5 years and suffering since 24.0 ± 3.05 years were recruited into the study from a schizophrenia rehabilitation center in Bengaluru. Methods All subjects were taking anti-psychotic medications and were in stable state for more than a month. Psychiatric medications were kept constant during the study period. Assessments were done at three points of time: (1) baseline, (2) after one month of usual routine (pre) and (3) after five months of validated Integrated Yoga (IY) intervention (post). Validated 1 h Yoga module (consisting of asanas, pranayama, relaxation techniques and chantings) was practiced for 5 months, five sessions per week. Antipsychotic-induced side effects were assessed using Simpson Angus Scale (SAS) and Udvalg for Kliniske Undersogelser (UKU) side effect rating scale. Cognitive functions (using Trail making Test A and B), clinical symptoms and anthropometry were assessed as secondary variables. Comparisons between "pre" and "post" data was done using paired samples t-tests after subtracting baseline scores from them respectively. Results At the end of five months, significant reduction in drug-induced Parkinsonian symptoms (SAS score; p=0.001) and 38 items of UKU scale was observed along with significant improvement in processing speed, executive functions and negative symptoms of schizophrenia patients. No side effects of Yoga were reported. Conclusions The present study provides preliminary evidence for usefulness of Integrated Yoga intervention in managing anti-psychotic-induced side effects.