Cognitive function is driven by dynamic interactions between large-scale neural circuits or networks, enabling behaviour. However, fundamental principles constraining these dynamic network processes have remained elusive. Here we use tools from control and network theories to offer a mechanistic explanation for how the brain moves between cognitive states drawn from the network organization of white matter microstructure. Our results suggest that densely connected areas, particularly in the default mode system, facilitate the movement of the brain to many easily reachable states. Weakly connected areas, particularly in cognitive control systems, facilitate the movement of the brain to difficult-to-reach states. Areas located on the boundary between network communities, particularly in attentional control systems, facilitate the integration or segregation of diverse cognitive systems. Our results suggest that structural network differences between cognitive circuits dictate their distinct roles in controlling trajectories of brain network function.

/pdf/controllability-of-structural-brain-networks-4yk12prurv.pdf

Controllability of structural brain networks.

Executive function performance in obesity and overweight individuals: A meta-analysis and review.

Examining the relationship between obesity and cognitive function: A systematic literature review

With rising rates of obesity, research continues to explore the contributions of homeostatic and hedonic mechanisms related to eating behaviour. In this Review, we synthesize the existing information on select biological mechanisms associated with reward-related food intake, dealing primarily with consumption of highly palatable foods. In addition to their established functions in normal feeding, three primary peripheral hormones (leptin, ghrelin and insulin) play important parts in food reward. Studies in laboratory animals and humans also show relationships between hyperphagia or obesity and neural pathways involved in reward. These findings have prompted questions regarding the possibility of addictive-like aspects in food consumption. Further exploration of this topic may help to explain aberrant eating patterns, such as binge eating, and provide insight into the current rates of overweight and obesity.

Hormonal and neural mechanisms of food reward, eating behaviour and obesity

Background. In this meta-analysis we review the findings from neuropsychological studies on set-shifting in people with eating disorders (EDs) or overweight/obesity. Method. Four databases (PubMed, PsycINFO, PSYNDEX and Web of Science) were searched for eligible studies. Effect sizes (ESs) were pooled using random-effects models. Moderator analyses were conducted for ED and overweight/obese subgroups, adult/adolescent samples and measures of set-shifting. Results. Sixty-four studies with a total of 1825 ED patients [1394 anorexia nervosa (AN), 376 bulimia nervosa (BN) and 55 binge eating disorder (BED)] and 10 studies with a total of 449 overweight/obese individuals were included. The meta-analysis revealed a small to medium ES for inefficient set-shifting across all three ED diagnoses (Hedges’ g = –0.45). Subgroup analyses yielded small to medium ESs for each ED subtype (g = –0.44 for AN, –0.53 for BED, –0.50 for BN), which did not differ significantly. There was a medium ES for restricting type AN (ANR; g = –0.51) but no significant ES for binge/purge type AN (AN/BP; g = –0.18). A medium ES was found across obesity studies (g = –0.61). The ES across overweight studies was not significant (g = –0.07). Adult samples did not differ from adolescent samples in either ED or overweight/obesity studies. The different set-shifting measures were associated with largely varying ESs. Conclusions. The meta-analysis provides strong support that inefficient set-shifting is a salient neuropsychological phenomenon across ED subtypes and obesity, but is less prominent in AN/BP and overweight. Compulsivity seems to be a common underlying factor supporting a dimensional and transdiagnostic conceptualization of EDs and obesity.

Set-shifting ability across the spectrum of eating disorders and in overweight and obesity: a systematic review and meta-analysis.

Obesity is a multifactorial disease caused by the interaction between genotype and environment, and it is considered to be a type of addictive alteration. The A1 allele of the DRD2/ANKK1-TaqIA gene has been associated with addictive disorders, with obesity and with the performance in executive functions. The 7 repeat allele of the DRD4 gene has likewise been associated with the performance in executive functions, as well as with addictive behaviors and impulsivity. Participants were included in the obesity group (N = 42) if their body mass index (BMI) was equal to or above 30, and in the lean group (N = 42) if their BMI was below 25. The DRD2/ANKK1-TaqIA and DRD4 VNTR polymorphisms were obtained. All subjects underwent neuropsychological assessment. Eating behavior traits were evaluated. The ‘DRD2/ANKK1-TaqIA A1-allele status’ had a significant effect on almost all the executive variables, but no significant ‘DRD4 7R-allele status’ effects were observed for any of the executive variables analyzed. There was a significant ‘group’ x ‘DRD2/ANKK1-TaqIA A1-allele status’ interaction effect on LN and ‘group’ x ‘DRD4 7R-allele status’ interaction effect on TMT B-A score. Being obese and a carrier of the A1 allele of DRD2/ANKK1-TaqIA or the 7R allele of DRD4 VNTR polymorphisms could confer a weakness as regards the performance of executive functions.

/pdf/dopamine-genes-drd2-ankk1-taqa1-and-drd4-7r-and-executive-2m3020skuj.pdf

Dopamine Genes (DRD2/ANKK1-TaqA1 and DRD4-7R) and Executive Function: Their Interaction with Obesity

Obesity is often accompanied with psychosocial adjustment problems, such as difficulties in social interactions and social withdrawal. A key aspect of social cognition is theory of mind, which allows inferring mental states, feelings, motivations, and beliefs of others and to use this information to predict their future behaviour. Theory of mind is highly dependent on prefrontal dopaminergic neurotransmission, which is regulated by catechol-O-methyltransferase (COMT) activity. We aimed at determining whether theory of mind is altered in obesity and if this ability is modulated by COMT. Fifty patients with obesity and 47 normal-weight individuals underwent the Reading the Mind in the Eyes Test, the Wisconsin Card Sorting Test, and the Vocabulary subscale of the Wechsler Adult Intelligence Scale. The genotype for the COMT Val 158 Met functional polymorphism was determined for all subjects. Patients with obesity obtained significantly lower scores in the negative items of the Reading the Mind in the Eyes Test than normal-weight subjects. Further, an interaction effect was observed between group and COMT genotype. Specifically, the presence of the Met allele was associated to a better identification of negative mental states only in patients with obesity. Our results indicate that obesity is accompanied with difficulties in theory of mind and that this ability is influenced by the COMT genotype.

/pdf/effect-of-the-catechol-o-methyltransferase-val-158-met-ipzr0uooxo.pdf

Effect of the catechol-O-methyltransferase Val 158 Met polymorphism on theory of mind in obesity.

The prevalence of obesity is increasing worldwide. Previous research has shown a relationship between obesity and both executive functioning alterations and frontal cortex volume reductions. The Brain Derived Neurotrophic Factor val66met polymorphism, involved in eating behavior, has also been associated with executive functions and prefrontal cortex volume, but to date it has not been studied in relation to obesity. Our aim is to elucidate whether the interaction between the Brain Derived Neurotrophic Factor val66met polymorphism and obesity status influences executive performance and frontal-subcortical brain structure. Sixty-one volunteers, 34 obese and 27 controls, age range 12–40, participated in the study. Participants were assigned to one of two genotype groups (met allele carriers, n = 16, or non-carriers, n = 45). Neuropsychological assessment comprised the Trail Making Test, the Stroop Test and the Wisconsin Card Sorting Test, all tasks that require response inhibition and cognitive flexibility. Subjects underwent magnetic resonance imaging in a Siemens TIM TRIO 3T scanner and images were analyzed using the FreeSurfer software. Analyses of covariance controlling for age and intelligence showed an effect of the obesity-by-genotype interaction on perseverative responses on the Wisconsin Card Sorting Test as well as on precentral and caudal middle frontal cortical thickness: obese met allele carriers showed more perseverations on the Wisconsin Card Sorting Test and lower frontal thickness than obese non-carriers and controls. In conclusion, the Brain Derived Neurotrophic Factor may play an important role in executive functioning and frontal brain structure in obesity. © 2014 Wiley Periodicals, Inc.

The interaction effect between BDNF val66met polymorphism and obesity on executive functions and frontal structure.

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Dopamine Genes (DRD2/ANKK1-TaqA1 and DRD4-7R) and Executive Function: Their Interaction with Obesity

Effect of the catechol-O-methyltransferase Val 158 Met polymorphism on theory of mind in obesity.

The interaction effect between BDNF val66met polymorphism and obesity on executive functions and frontal structure.