This paper systematically reviews the literature pertaining to the use of resting-state functional magnetic resonance imaging (rsfMRI) in anorexia nervosa (AN), classifying studies on the basis of different analysis approaches. We followed PRISMA guidelines. Fifteen papers were included, investigating a total of 294 participants with current or past AN and 285 controls. The studies used seed-based, whole-brain independent component analysis (ICA), network-of-interest ICA based and graph analysis approaches. The studies showed relatively consistent overlap in results, yet little overlap in their analytical approach and/or a-priori assumptions. Functional connectivity alterations were mainly found in the corticolimbic circuitry, involved in cognitive control and visual and homeostatic integration. Some overlapping findings were found in brain areas putatively important in AN, such as the insula. These results suggest altered functional connectivity in networks/areas linked to the main symptom domains of AN, such as impaired cognitive control and body image disturbances. These preliminary evidences suggest that more targeted treatments need to be developed that focus on these two symptom domains. Further studies with multi-approach analyses and longitudinal designs are needed to better understand the complexity of AN.

Background Studies of mitochondrial morphology vary in techniques. Most use one morphological parameter while others describe mitochondria qualitatively. Because mitochondria are so dynamic, a single parameter does not capture the true state of the network and may lead to erroneous conclusions. Thus, a gestalt method of analysis is warranted. New Method This work describes a method combining immunofluorescence assays with computerized image analysis to measure the mitochondrial morphology within neuritic projections of a specific population of neurons. Six parameters of mitochondrial morphology were examined utilizing ImageJ to analyze colocalized signals. Results Using primary neuronal cultures from Drosophila, we tested mitochondrial morphology in neurites of dopaminergic (DA) neurons. We validate our model using mutants with known defects in mitochondrial morphology. Furthermore, we show a difference in mitochondrial morphology between cells treated as control or with a neurotoxin inducing PD (Parkinson's Disease in humans)-like pathology. We also show interactions between morphological parameters and experimental treatment. Comparison with Existing Methods Our method is a significant improvement of previously described methods. Six morphometric parameters are quantified, providing a gestalt analysis of mitochondrial morphology. Also it can target specific populations of mitochondria using immunofluorescence assay and image analysis. Conclusions We found that our method adequately detects differences in mitochondrial morphology between treatment groups. We conclude that some parameters may be unique to a mutation or a disease state, and the relationship between parameters is altered by experimental treatment. We suggest at least four variables should be considered when using mitochondrial structure as an experimental endpoint.

ObjectivesImpulsivity is a vulnerability trait for poor self-regulation in substance use disorder (SUD). Working memory (WM) training improves impulsivity and self-regulation in psychiatric disorders. Here we test WM training in methamphetamine use disorder (MUD).MethodsThere are 15 MUD patients receiving inpatient treatment as usual (TAU) and 20 who additionally completed WM cognitive training (CT) and 25 healthy controls (HC). MANCOVA repeated measures analyses examined changes in impulsivity and self-regulation at baseline and after 4 weeks.ResultsPost hoc t tests confirmed that at baseline, feelings of self-control were significantly lower in the MUD (t = 2.001, p = 0.05) and depression was higher (t = 4.980, p = 0.001), as was BIS total impulsivity (t = 5.370, p = 0.001) compared to the HC group. Total self-regulation score was higher in HC than MUD patients (t = 5.370, p = 0.001). CT had a 35% learning rate (R 2 = 0.3523, p < 0.05). Compared to follow-up TAU, follow-up CT group had higher self-reported mood scores (t = 2.784, p = 0.01) and higher compared to CT baseline (t = 2.386, p = 0.036). Feelings of self-control were higher in CT than TAU at follow-up (t = 2.736, p = 0.012) and also compared to CT baseline (t = 3.390, p = 0.006), lack of planning significantly improved in CT between baseline and follow-up (t = 2.219, p = 0.048), as did total impulsivity scores (t = 2.085, p = 0.048). Measures of self-regulation were improved in the CT group compared to TAU at follow-up, in total score (t = 2.442, p = 0.038), receiving score (t = 2.314, p = 0.029) and searching score (t = 2.362, p = 0.027). Implementing self-regulation was higher in the CT group compared to TAU (t = 2.373, p = 0.026).ConclusionsWM training may improve control of impulsivity and self-regulation in people with MUD.

Drosophila melanogaster is widely used to study genetic factors causing Parkinson’s disease (PD) due largely to the use of sophisticated genetic approaches and the presence of a high conservation of gene sequence/function between Drosophila and mammals. However, in Drosophila little has been done to study the environmental factors which cause over 90% of PD cases. We used Drosophila primary neuronal culture to study degenerative effects of a well-known PD toxin MPP+. DA neurons were selectively degenerated by MPP+ whereas cholinergic and GABAergic neurons were not affected. This DA neuronal loss was due to post-mitotic degeneration, not by inhibition of DA neuronal differentiation. We also found that MPP+-mediated neurodegeneration was rescued by D2 agonists quinpirole and bromocriptine. This rescue was through activation of Drosophila D2 receptor DD2R, as D2 agonists failed to rescue MPP+-toxicity in neuronal cultures prepared from both a DD2R deficiency line and a transgenic line pan-neuronally expressing DD2R RNAi. Furthermore, DD2R autoreceptors in DA neurons played a critical role in the rescue. When DD2R RNAi was expressed only in DA neurons, MPP+ toxicity was not rescued by D2 agonists. Our study also showed that rescue of DA neurodegeneration by Drosophila DD2R activation was mediated through suppression of action potentials in DA neurons.

Understanding how genetics influences obesity, brain activity and eating behaviour will add important insight for developing strategies for weight-loss treatment, as obesity may stem from different causes and as individual feeding behaviour may depend on genetic differences. To this end, we examined how an obesity risk allele for the FTO gene affects brain activity in response to food images of different caloric content via functional magnetic resonance imaging (fMRI). Thirty participants homozygous for the rs9939609 single nucleotide polymorphism were shown images of low- or high-calorie food while brain activity was measured via fMRI. In a whole-brain analysis, we found that people with the FTO risk allele genotype (AA) had increased activity compared with the non-risk (TT) genotype in the posterior cingulate, cuneus, precuneus and putamen. Moreover, higher body mass index in the AA genotype was associated with reduced activity to food images in areas important for emotion (cingulate cortex), but also in areas important for impulse control (frontal gyri and lentiform nucleus). Lastly, we corroborate our findings with behavioural scales for the behavioural inhibition and activation systems. Our results suggest that the two genotypes are associated with differential neural processing of food images, which may influence weight status through diminished impulse control and reward processing.