COX-2 in the neurodegenerative process of Parkinson's disease

Copyright © 2012 International Union of Biochemistry and Molecular Biology, Inc.Peer reviewedPublisher PD

Appetitive traits and relationships with BMI in adults: Development of the Adult Eating Behaviour Questionnaire

The Child Eating Behaviour Questionnaire (CEBQ) is a validated parent-report measure of appetitive traits associated with weight in childhood. There is currently no matched measure for use in adults. The aim of this study was to adapt the CEBQ into a self-report Adult Eating Behaviour Questionnaire (AEBQ) to explore whether the associations between appetitive traits and BMI observed in children are present in adults. Two adult samples were recruited one year apart from an online survey panel in 2013 (n = 708) and 2014 (n = 954). Both samples completed the AEBQ and self-reported their weight and height. Principal component analysis (PCA) was used to derive 35 items for the AEBQ in Sample 1 and confirmatory factor analysis (CFA) was used to replicate the factor structure in Sample 2. Reliability of the AEBQ was assessed using Cronbach’s α and a two week test-retest in a sub-sample of 93 participants. Correlations between appetitive traits measured by the AEBQ and BMI were calculated. PCA and CFA results showed the AEBQ to be a reliable questionnaire (Cronbach’s α > 0.70) measuring 8 appetitive traits similar to the CEBQ [Hunger (H), Food Responsiveness (FR), Emotional Over-Eating (EOE), Enjoyment of Food (EF), Satiety Responsiveness (SR), Emotional Under-eating (EUE), Food Fussiness (FF) and Slowness in Eating (SE)]. Associations with BMI showed FR, EF (p < 0.05) and EOE (p < 0.01) were positively associated and SR, EUE and SE (p < 0.01) were negatively associated. Overall, the AEBQ appears to be a reliable measure of appetitive traits in adults which translates well from the validated child measure. Adults with a higher BMI had higher scores for ‘food approach’ traits (FR, EOE and EF) and lower scores for ‘food avoidance’ traits (SR, EUE and SE)

Examining the validity and consistency of the Adult Eating Behaviour Questionnaire-Español (AEBQ-Esp) and its relationship to BMI in a Mexican population

Purpose: Appetitive traits in adults and their associations with weight can be measured using the Adult Eating Behaviour Questionnaire (AEBQ). The aim of this study was to confirm the factor structure of the Spanish AEBQ (AEBQ-Esp) in a Mexican sample and explore associations between the eight traits with body mass index (BMI). Method: A sample of 1023 adults, mean age of 36.8 ± 12.8 years, was recruited from Guadalajara, Mexico. Researchers weighed and measured participants, and they completed the AEBQ-Esp either online or in paper format and reported sociodemographic data. To test two alternative factor structures (eight factors including Hunger; seven factors excluding Hunger), confirmatory factor analysis (CFA) was used. Internal reliability was assessed using Cronbach’s alpha; test–retest reliability was assessed using intra-class correlation coefficients. Multivariate linear regressions were used to test for associations between the AEBQ subscales and BMI, adjusted for age, sex, format of AEBQ responses, education, marital and employment status. Results: A seven-factor structure was the best model fit using CFA, excluding the Hunger subscale but similar to the original AEBQ. Internal reliability was good for all subscales (Cronbach’s α = 0.70–0.86), and the intra-class correlation coefficient (0.70–0.91) reflected good test–retest reliability. In the fully adjusted models, Satiety Responsiveness [β = − 0.61; (− 1.01, − 0.21)] and Slowness in Eating [β = − 0.70; (− 1.01, − 0.39)] were negatively associated with BMI, and Emotional Over-Eating [β = 0.94; (0.62, 1.27)] was positively associated with BMI. Conclusions: The AEBQ-Esp (excluding Hunger) appears to be a valid and reliable psychometric questionnaire for measuring appetitive traits in a Mexican Spanish-speaking population. Some traits appear to be associated with BMI in adulthood and warrant further exploration. Level of evidence: Level III evidence obtained from well-designed cohort or case–control analytic studies. Although this was just an observational study, it was well designed and provided new evidence

The interpretation of low mood and worry by high users of secondary care with medically unexplained symptoms

DA - 20111021 IS - 1471-2296 (Electronic) IS - 1471-2296 (Linking) LA - eng PT - Journal Article SB - IMPeer reviewedPublisher PD

Apoptosis Signal-Regulating Kinase 1 Mediates MPTP Toxicity and Regulates Glial Activation

Apoptosis signal-regulating kinase 1 (ASK1), a member of the mitogen-activated protein kinase 3 family, is activated by oxidative stress. The death-signaling pathway mediated by ASK1 is inhibited by DJ-1, which is linked to recessively inherited Parkinson's disease (PD). Considering that DJ-1 deficiency exacerbates the toxicity of the mitochondrial complex I inhibitor 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we sought to investigate the direct role and mechanism of ASK1 in MPTP-induced dopamine neuron toxicity. In the present study, we found that MPTP administration to wild-type mice activates ASK1 in the midbrain. In ASK1 null mice, MPTP-induced motor impairment was less profound, and striatal dopamine content and nigral dopamine neuron counts were relatively preserved compared to wild-type littermates. Further, microglia and astrocyte activation seen in wild-type mice challenged with MPTP was markedly attenuated in ASK1−/− mice. These data suggest that ASK1 is a key player in MPTP-induced glial activation linking oxidative stress with neuroinflammation, two well recognized pathogenetic factors in PD. These findings demonstrate that ASK1 is an important effector of MPTP-induced toxicity and suggest that inhibiting this kinase is a plausible therapeutic strategy for protecting dopamine neurons in PD

Appetitive Traits associated with Higher and Lower Body Mass Index: Evaluating the Validity of the Adult Eating Behaviour Questionnaire in an Australian Sample

Background: The aims of this study were to evaluate the factor structure of the newly developed Adult Eating Behaviour Questionnaire (AEBQ) (Hunot et al., Appetite 105:356-63, 2016) in an Australian sample, and examine associations between the four food approach and four food avoidance appetitive traits with body mass index (BMI). Methods: Participants (N = 998) recruited between May and October 2016 via a university research participation scheme and online social network sites completed an online version of the AEBQ and self-reported demographic and anthropometric data. Of the sample, 84.8% were females, 29.6% had completed a university degree and the overall mean age was 24.32 years (SD = 8.32). Confirmatory factor analysis (CFA) was used to test three alternative factor structures (derived from issues raised in the original development study): the original 8 factor model, a 7 factor model with Food Responsiveness and Hunger scales combined, and a 7 factor model with the Hunger scale removed. Results: The CFA revealed that the original 8 factor model was a better fit to the data than the 7 factor model in which Food Responsiveness and Hunger scales were combined. However, while reliability estimates for 7 of the 8 scales were good (Cronbach’s α between 0.70-0.86), the reliability of the Hunger scale was modest (0.67) and dropping this factor resulted in a good fitting model. All food avoidance scales (except Food Fussiness) were negatively associated with body mass index (BMI) whereas Emotional Overeating was the only food approach scale positively associated with BMI. Conclusions: The study supports the use of the AEBQ as a reliable and valid measure of food approach and avoidance appetitive traits in adults. Longitudinal studies that examine continuity and stability of appetitive traits across the lifespan will be facilitated by the addition of this measurement tool to the literature

Behavioural Susceptibility Theory: Professor Jane Wardle and the Role of Appetite in Genetic Risk of Obesity

Purpose of Review: There is considerable variability in human body weight, despite the ubiquity of the 'obesogenic' environment. Human body weight has a strong genetic basis and it has been hypothesised that genetic susceptibility to the environment explains variation in human body weight, with differences in appetite being implicated as the mediating mechanism; so-called 'behavioural susceptibility theory' (BST), first described by Professor Jane Wardle. This review summarises the evidence for the role of appetite as a mediator of genetic risk of obesity. Recent Findings: Variation in appetitive traits is observable from infancy, drives early weight gain and is highly heritable in infancy and childhood. Obesity-related common genetic variants identified through genome-wide association studies show associations with appetitive traits, and appetite mediates part of the observed association between genetic risk and adiposity. Summary: Obesity results from an interaction between genetic susceptibility to overeating and exposure to an 'obesogenic' food environment

Development and validation of the Self-Regulation of Eating Behaviour Questionnaire for adults

Background Eating self-regulatory capacity can help individuals to cope with the obesogenic environment and achieve, as well as maintain, a healthy weight and diet. At present, there is no comprehensive, reliable and valid questionnaire for assessing this capacity and measuring change in response to self-regulation interventions in adults. This paper reports the development of the Self-regulation of Eating Behaviour Questionnaire (SREBQ) for use in UK adults, and presents evidence for its reliability and construct validity. The development of the SREBQ involved generation of an item pool, followed by two pilot studies (Samples 1 and 2) and a test of the questionnaire’s underlying factor structure (Sample 3). The final version of the SREBQ was then assessed for reliability and construct validity (Sample 4). Results Development of the SREBQ resulted in a 5-item questionnaire. The face validity was satisfactory, as assessed by the pilot studies. The factor structure analysis (Sample 3) suggested that it has a single underlying factor, which was confirmed in a second sample (Sample 4). The SREBQ had strong construct validity, showing a positive correlation with general measures of self-regulation. It was also positively correlated with motivation and behavioural automaticity, and negatively correlated with food responsiveness and emotional over-eating (p < 0.001). It showed good discriminant validity, as it was only weakly associated with satiety responsiveness, food fussiness and slowness in eating. Conclusions The SREBQ is a reliable and valid measure for assessment of eating self-regulatory capacity in the general UK adult population

Glucocorticoid receptor in astrocytes regulates midbrain dopamine neurodegeneration through connexin hemichannel activity

The precise contribution of astrocytes in neuroinflammatory process occurring in Parkinson's disease (PD) is not well characterized. In this study, using GR(Cx30CreERT2) mice that are conditionally inactivated for glucocorticoid receptor (GR) in astrocytes, we have examined the actions of astrocytic GR during dopamine neuron (DN) degeneration triggered by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The results show significantly augmented DN loss in GR(Cx30CreERT2) mutant mice in substantia nigra (SN) compared to controls. Hypertrophy of microglia but not of astrocytes was greatly enhanced in SN of these astrocytic GR mutants intoxicated with MPTP, indicating heightened microglial reactivity compared to similarly-treated control mice. In the SN of GR astrocyte mutants, specific inflammation-associated transcripts ICAM-1, TNF-alpha and Il-1 beta as well as TNF-alpha protein levels were significantly elevated after MPTP neurotoxicity compared to controls. Interestingly, this paralleled increased connexin hemichannel activity and elevated intracellular calcium levels in astrocytes examined in acute midbrain slices from control and mutant mice treated with MPP+. The increased connexin-43 hemichannel activity was found in vivo in MPTP-intoxicated mice. Importantly, treatment of MPTP-injected GR(Cx30CreERT2) mutant mice with TAT-Gap19 peptide, a specific connexin-43 hemichannel blocker, reverted both DN loss and microglial activation; in wild-type mice there was partial but significant survival effect. In the SN of postmortem PD patients, a significant decrease in the number of astrocytes expressing nuclear GR was observed, suggesting the participation of astrocytic GR deregulation of inflammatory process in PD. Overall, these data provide mechanistic insights into GR-modulated processes in vivo, specifically in astrocytes, that contribute to a pro-inflammatory state and dopamine neurodegeneration in PD pathology